Magnetization plateaus in the antiferromagnetic Ising chain with single-ion anisotropy and quenched disorder.

We have studied the presence of plateaus on the low-temperature magnetization of an antiferromagnetic spin-1 chain, as an external uniform magnetic field is varied. A crystal-field interaction is present in the model and the exchange constants follow a random quenched (Bernoulli or Gaussian) distribution. Using a transfer-matrix technique we calculate the largest Lyapunov exponent and, from it, the magnetization at low temperatures as a function of the magnetic field, for different values of the crystal field and the width of the distributions. For the Bernoulli distribution, the number of plateaus increases, with respect to the uniform case [Litaiff et al., Solid State Commun. 147, 494 (2008)] and their presence can be linked to different ground states, when the magnetic field is varied. For the Gaussian distributions, the uniform scenario is maintained, for small widths, but the plateaus structure disappears as the width increases.

Magnetic properties and critical behavior of disordered Fe(1-x)Ru(x) alloys: a Monte Carlo approach.

We study the critical behavior of a quenched random-exchange Ising model with competing interactions on a bcc lattice. This model was introduced in the study of the magnetic behavior of Fe(1-x)Ru(x) alloys for ruthenium concentrations x=0%, x=4%, x=6%, and x=8%. Our study is carried out within a Monte Carlo approach, with the aid of a re-weighting multiple histogram technique. By means of a finite-size scaling analysis of several thermodynamic quantities, taking into account up to the leading irrelevant scaling field term, we find estimates of the critical exponents α, ß, γ, and ν, and of the critical temperatures of the model. Our results for x=0% are in excellent agreement with those for the three-dimensional pure Ising model in the literature. We also show that our critical exponent estimates for the disordered cases are consistent with those reported for the transition line between paramagnetic and ferromagnetic phases of both randomly dilute and ±J Ising models. We compare the behavior of the magnetization as a function of temperature with that obtained by Paduani and Branco (2008), qualitatively confirming the mean-field result. However, the comparison of the critical temperatures obtained in this work with experimental measurements suggest that the model (initially obtained in a mean-field approach) needs to be modified.

Mean-field calculation of critical parameters and log-periodic characterization of an aperiodic-modulated model.

We employ a mean-field approximation to study the Ising model with aperiodic modulation of its interactions in one spatial direction. Two different values for the exchange constant, J(A) and J(B), are present, according to the Fibonacci sequence. We calculate the pseudocritical temperatures for finite systems and extrapolate them to the thermodynamic limit. We explicitly obtain the exponents ß, δ, and γ and, from the usual scaling relations for anisotropic models at the upper critical dimension (assumed to be 4 for the model we treat), we calculate α, ν, ν(∥), η, and η(∥). Within the framework of a renormalization-group approach, the Fibonacci sequence is a marginal one and we obtain exponents that depend on the ratio r≡J(B)/J(A), as expected; however, the scaling relation γ=ß(δ-1) is obeyed for all values of r we studied. We characterize some thermodynamic functions as log-periodic functions of their arguments, as expected for aperiodic-modulated models, and obtain precise values for the exponents from this characterization.

Noise-induced duodenal lesions: a light and electron microscopy study of the lesions of the rat duodenal mucosa exposed to low frequency noise.

BACKGROUND AND AIMS: Non-auditory effects of noise, including digestive disorders have long being reported. Low frequency noise (LFN) is considered to be responsible to most of non-auditory effects of noise and is widely spread in modern societies. Only a few studies were designed to evaluate these noise-induced digestive alterations. The pathogenesis of duodenal ulcers and erosions is complex and noise may be an environmental co-factor. The aim of the present study was to investigate the morphological injury of LFN-exposed duodenal mucosa. MATERIALS AND METHODS: Five groups of Wistar rats were exposed to continuous LFN, during increasing periods, since 1 to 13 weeks. A control group was kept in silence. Duodenal specimens were studied using light microscopy (LM), scanning electron microscopy (SEM) and transmission electron microscopy (TEM). RESULTS: We disclosed several changes in LFN-exposed rats: on LM, mucosa showed superficial erosions of the epithelial layer, degeneration, picnosis and cell death, with no inflammation. On SEM, epithelium presented displacement of cells and unequal distribution of microvilli, with coalescence and fusion. On TEM, microvilli were irregularly distributed, damaged and fragmented. The terminal web was destroyed. Morphological alterations occurred early, after just 1 week of LFN-exposure, persisted with longer noise exposition and did not suffer any evolution. Changes were similar among all LFN-exposed groups. CONCLUSIONS: LFN-exposed duodenal mucosa develops destruction of microvilli and terminal web, leading to cellular death and development of superficial erosions. These lesions of cytoskeleton structures could explain why cells with actinic and tubulinic structures like cilia and microvilli present severe destruction after LFN-exposure. These erosions are similar to those seen in dyspeptic patients.

Influence of aperiodic modulations on first-order transitions: numerical study of the two-dimensional Potts model.

We study the Potts model on a rectangular lattice with aperiodic modulations in its interactions along one direction. Numerical results are obtained using the Wolff algorithm and for many lattice sizes, allowing for a finite-size scaling analyses to be carried out. Three different self-dual aperiodic sequences are employed, which leads to more precise results, since the exact critical temperature is known. We analyze two models, with 6 and 15 number of states: both present first-order transitions on their uniform versions. We show that the Harris-Luck criterion, originally introduced in the study of continuous transitions, is obeyed also for first-order ones. Also, we show that the new universality class that emerges for relevant aperiodic modulations depends on the number of states of the Potts model, as obtained elsewhere for random disorder, and on the aperiodic sequence. We determine the occurrence of log-periodic behavior, as expected for models with aperiodic modulated interactions.

Anisotropic Heisenberg model on hierarchical lattices with aperiodic interactions: a renormalization-group approach.

Using a real-space renormalization-group approximation, we study the anisotropic quantum Heisenberg model on hierarchical lattices, with interactions following aperiodic sequences. Three different sequences are considered, with relevant and irrelevant fluctuations, according to the Luck-Harris criterion. The phase diagram is discussed as a function of the anisotropy parameter Delta (such that Delta=0 and 1 correspond to the isotropic Heisenberg and Ising models, respectively). We find three different types of phase diagrams, with general characteristics: the isotropic Heisenberg plane is always an invariant one (as expected by symmetry arguments) and the critical behavior of the anisotropic Heisenberg model is governed by fixed points on the Ising-model plane. Our results for the isotropic Heisenberg model show that the relevance or irrelevance of aperiodic models, when compared to their uniform counterpart, is as predicted by the Harris-Luck criterion. A low-temperature renormalization-group procedure was applied to the classical isotropic Heisenberg model in two-dimensional hierarchical lattices: the relevance criterion is obtained, again in accordance with the Harris-Luck criterion.

Nonuniversal behavior for aperiodic interactions within a mean-field approximation.

We study the spin-1/2 Ising model on a Bethe lattice in the mean-field limit, with the interaction constants following one of two deterministic aperiodic sequences, the Fibonacci or period-doubling one. New algorithms of sequence generation were implemented, which were fundamental in obtaining long sequences and, therefore, precise results. We calculate the exact critical temperature for both sequences, as well as the critical exponents beta, gamma, and delta . For the Fibonacci sequence, the exponents are classical, while for the period-doubling one they depend on the ratio between the two exchange constants. The usual relations between critical exponents are satisfied, within error bars, for the period-doubling sequence. Therefore, we show that mean-field-like procedures may lead to nonclassical critical exponents.

Variational-method study of the spin-1 Ising model with biaxial crystal-field anisotropy.

The phase diagram of the spin-1 Ising model in the presence of a biaxial crystal-field anisotropy is studied within the framework of a variational approach, based on the Bogolyubov inequality for the free energy. We have investigated the effects of a transverse crystal field Dy on the phase diagram in the T-Dx plane. Results obtained by using effective-field theory (EFT) on the honeycomb (z=3), square (z=4), and simple cubic (z=6) lattices (z is the coordination number) show only continuous phase transitions, while the variational approach presents first-order and continuous phase transitions for Dy=0. We have also used the EFT for larger values of z and we observe the presence of tricritical points in the phase diagrams, for z>or=7, in accordance with the variational approach results.

Low-frequency noise effects on the parotid gland of the Wistar rat.

BACKGROUND: Long-term low-frequency noise (LFN) (

Noise-induced duodenal lesions

Vibroacoustic disease (VAD) is a systemic diseasethat results from long-term exposure tolow-frequency noise (LFN). VAD can cause lesionsin several organs. Noise-exposed individualsfrequently present digestive symptoms, butonly a few studies have attempted to evaluategastrointestinal lesions. The aim of this studywas to investigate the duodenal alterations inVAD, using an animal model of the disease.Adult Wistar rats were exposed to continuousLFN. After five, nine and thirteen weeks theywere sacrificed. The duodenums were studiedby light microscopy and scanning electron microscopy,and compared with those of animalskept in silence. Superficial erosions and widespreadcell death with microvilli coalescence andfusion were observed, by light and electronmicroscopy. Erosion, cellular degeneration anddeath, and microvilli destruction, reflect noise-inducedduodenal alterations in rats which may beequivalent to the ulcers and dyspeptic symptomsreported in human VAD patients (AU)

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Effects of anisotropy on a quantum Heisenberg spin glass on a three-dimensional hierarchical lattice.

We study the anisotropic Heisenberg spin-glass model on a three-dimensional hierarchical lattice (designed to approximate the cubic lattice), within a real-space renormalization-group approach. Two different initial probability distributions for the exchange interaction (Jij), Gaussian and uniform, are used, with zero mean and width J. The (kT/J) x Delta0 phase diagram is obtained, where T is the temperature, Delta0 is the first moment of the probability distribution for the uniaxial anisotropy, and k is the Boltzmann constant. For the Ising model (Delta0 = 1), there is a spin-glass phase at low temperatures (high J) and a paramagnetic phase at high temperatures (low J). For the isotropic Heisenberg model (Delta0 = 0), our results indicate no spin-glass phase at finite temperatures. The transition temperature between the spin-glass and paramagnetic phase decreases with Delta0, as expected, but goes to zero at a finite value of the anisotropy parameter, namely Delta0 = Deltac approximately 0.59. Our results indicate that the whole transition line, between the paramagnetic and the spin-glass phases, for Deltac < Delta0 < 1, belongs to the same universality class as the transition for the Ising spin glass.

Vibroacoustic disease.

Vibroacoustic disease (VAD) is a whole-body, systemic pathology, characterized by the abnormal proliferation of extra-cellular matrices, and caused by excessive exposure to low frequency noise (LFN). VAD has been observed in LFN-exposed professionals, such as, aircraft technicians, commercial and military pilots and cabin crewmembers, ship machinists, restaurant workers, and disk-jockeys. VAD has also been observed in several populations exposed to environmental LFN. This report summarizes what is known to date on VAD, LFN-induced pathology, and related issues. In 1987, the first autopsy of a deceased VAD patient was performed. The extent of LFN induced damage was overwhelming, and the information obtained is, still today, guiding many of the associated and ongoing research projects. In 1992, LFN-exposed animal models began to be studied in order to gain a deeper knowledge of how tissues respond to this acoustic stressor. In both human and animal models, LFN exposure causes thickening of cardiovascular structures. Indeed, pericardial thickening with no inflammatory process, and in the absence of diastolic dysfunction, is the hallmark of VAD. Depressions, increased irritability and aggressiveness, a tendency for isolation, and decreased cognitive skills are all part of the clinical picture of VAD. LFN is a demonstrated genotoxic agent, inducing an increased frequency of sister chromatid exchanges in both human and animal models. The occurrence of malignancies among LFN-exposed humans, and of metaplastic and displastic appearances in LFN-exposed animals, clearly corroborates the mutagenic outcome of LFN exposure. The inadequacy of currently established legislation regarding noise assessments is a powerful hindrance to scientific advancement. VAD can never be fully recognized as an occupational and environmental pathology unless the agent of disease--LFN--is acknowledged and properly evaluated. The worldwide suffering of LFN-exposed individuals is staggering and it is unethical to maintain this status quo.

Low frequency noise and whole-body vibration cause increased levels of sister chromatid exchange in splenocytes of exposed mice.

Chronic exposure to low frequency (LF) noise and whole-body vibration (WBV) induces both physiological and psychological alterations in man. Recently, we have shown that long-term occupational exposure to LF noise and WBV produces genotoxic effects in man expressed as an increase in sister chromatid exchange (SCE) levels in lymphocytes. The objectives of the present study were to investigate whether the observed effect could be reproduced in a murine model and, if so, which of the agents, LF noise alone or in combination with WBV, would be instrumental in the SCE induction. SCEs were analyzed in spleen lymphocytes of mice exposed to LF noise alone and in combination with WBV for 300 and 600 hr. An effect at the cell cycle kinetics level was also investigated. The results revealed significant increases in the mean SCE number per cell and in the proportion of cells with high frequency of SCEs (HFCs) in lymphocytes of mice submitted to combined noise and WBV over controls. No significant differences were found between single noise-exposed and control mice. A cell cycle delay was observed exclusively in the noise and WBV exposure groups. In conclusion, we demonstrated that, as in exposed workers, prolonged exposure to the combination of LF noise and WBV determines an increase in SCE level in mice while LF noise alone is not effective in SCE induction.

Genetic variation in the 5q31 cytokine gene cluster confers susceptibility to Crohn disease.

Linkage disequilibrium (LD) mapping provides a powerful method for fine-structure localization of rare disease genes, but has not yet been widely applied to common disease. We sought to design a systematic approach for LD mapping and apply it to the localization of a gene (IBD5) conferring susceptibility to Crohn disease. The key issues are: (i) to detect a significant LD signal (ii) to rigorously bound the critical region and (iii) to identify the causal genetic variant within this region. We previously mapped the IBD5 locus to a large region spanning 18 cM of chromosome 5q31 (P<10(-4)). Using dense genetic maps of microsatellite markers and single-nucleotide polymorphisms (SNPs) across the entire region, we found strong evidence of LD. We bound the region to a common haplotype spanning 250 kb that shows strong association with the disease (P< 2 x 10(-7)) and contains the cytokine gene cluster. This finding provides overwhelming evidence that a specific common haplotype of the cytokine region in 5q31 confers susceptibility to Crohn disease. However, genetic evidence alone is not sufficient to identify the causal mutation within this region, as strong LD across the region results in multiple SNPs having equivalent genetic evidence-each consistent with the expected properties of the IBD5 locus. These results have important implications for Crohn disease in particular and LD mapping in general.

In utero and postnatal exposure of Wistar rats to low frequency/high intensity noise depletes the tracheal epithelium of ciliated cells.

Chronic exposure of men or rodents to low frequency/high intensity (LFHI) noise causes a number of systemic changes that make up the so-called vibroacoustic disease (VAD), a disorder that includes alterations of the respiratory system, namely, of its epithelial layer. We have investigated here the susceptibility of the tracheal epithelium of Wistar rats to in utero and postnatal exposure to LFHI noise by comparing its ultrastructure with that of the tracheal epithelium of control rats and of animals exposed to LFHI noise only after reaching adulthood (8 weeks of age). Scanning electron microscopy (SEM) of the inner surface of rat trachea was used to determine the relative areas covered by ciliated and non-ciliated cells. In rats that were exposed in utero and postnatally to LFHI noise, we observed that out of 100 microm(2) of tracheal epithelium only 31 +/- 14 microm(2) were covered by cilia, whereas in control rats; ciliated cells occupied an average of 60 +/- 18 microm(2) out of 100 microm(2) of the epithelium; this difference between the two groups was statistically significant (p <0.05). In rats that were exposed to LFHI noise only after reaching adulthood, cilia covered 55 +/- 22 microm(2) out of 100 microm(2) of the luminal surface of the trachea, a value that, although lower than that of controls, was not found to be statistically different. We conclude that (1) the tracheal ciliated cells are damaged by exposure of rats to LFHI noise if the animals are kept under this environmental aggression during in utero and postnatal periods; (2) tracheal ciliated cells from adult rats are more resistant to the deleterious effects of LFHI noise than pleura or lung alveolar cells that were shown before to undergo marked changes upon chronic exposure of rats to LFHI noise. These findings suggest a note of caution regarding pregnant women and young children: they should be prevented from areas where LFHI noise occurs, namely, in aircraft and textile industries where this type of environmental hazard is often present.

Increased levels of sister chromatid exchanges in military aircraft pilots.

Sister chromatid exchanges (SCEs) were scored in lymphocytes of nine high-performance pilots of alphajet aircrafts and of ten control individuals from the same air base. Statistical analysis of the mean SCE count per cell in the total number of cells analyzed as well as in those having 12 or more SCEs (high-frequency cells, HFCs) revealed a significant difference between pilots and controls, after adjusting for the effect of smoking. Analysis of the cell cycle kinetic data (replication and mitotic indices) revealed no significant differences either between pilots and controls or between smokers and nonsmokers. Previously, we reported an increase in the SCE levels in workers of the aeronautical industry exposed to noise and whole-body vibration. The present results corroborate those findings and indicate that noise and whole-body vibration may cause genotoxic effects in man.

The vibroacoustic disease--an emerging pathology.

Vibroacoustic disease (VAD) is the clinical manifestation of a systemic disease that develops after long-term exposure to noise (> or = 10 yr) which is characterized by large pressure amplitude (> or = 90 dB SPL) within the lower frequency bands (< or = 500 Hz). Noisy environments produce more widespread systemic effects than initially suspected. This paper describes the chronology, population studied, and the statistical treatment used in our studies of VAD over the past 20 yr. We also describe the motivation that led to the evaluation and assessment of the exposed employees. Future research aims are also discussed.

Noise assessment during aircraft run-up procedures.

BACKGROUND: A comprehensive noise survey was conducted at Oficinas Gerais de Material Aeronautico (OGMA), Alverca, Portugal, and at several Portuguese Air Force (PoAF) bases, as part of an ongoing occupational noise assessment program. The major objectives consisted of measuring and analyzing noise radiated by various types of military aircraft while undergoing maintenance, repair, or testing. METHODS: Amplitude, frequency, time history and statistical analysis were conducted on noise emitted by aircraft during run-up procedures. Analysis and evaluation used various noise indexes (Leq and Lmax), frequency spectra, and sound pressure time histories for the assessment of noise exposure on the employees during their working life span. RESULTS: The results show a predominance of large pressure amplitudes within the lower frequency bands. This was correlated with long-term clinical observations in these workers. This study corroborates the definition of vibroacoustic disease as a systemic, noise-induced occupational pathology caused by long-term (>10 yr) exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) noise.

A unique case of vibroacoustic disease: a tribute to an extraordinary patient.

This paper describes the case of a patient, Mr. A, who died in 1987. The information provided by Mr. A in life, and his insistence on making a will demanding an autopsy on his death, has given us invaluable data on Vibroacoustic Disease (VAD). Mr. A was an intellectually curious man who researched the medical literature related to his condition, and compared it to his own experience. He would describe all his sensations during his many epileptic seizures. Solely because of the results of Mr. A's autopsy, new avenues of research were initiated. These have led to new concepts and exciting new perspectives on noise-induced extraaural pathology. VAD is today a well-established and easily diagnosed entity. This paper is a tribute to Mr. A, in whose honor we have an on-going commitment to establish VAD as an occupational disease, reimbursable by Worker's Compensation.

The clinical stages of vibroacoustic disease.

BACKGROUND: Vibroacoustic disease (VAD) is an occupational disease occurring in susceptible workers who have had long-term exposure (> or = 10 yr) to large pressure amplitude (> or =90 dB SPL) and low frequency noise (< or = 500 Hz). The clinical progression is insidious, and lesions are found in many systems throughout the body. Some of the findings, such as extracellular matrix changes, appear to be specific to this disease. Others, such as cognitive impairment, seem to be common in different types of stress-induced pathology. In 1956, Professor Eugenia Andreeva-Galanina developed a classification of hand-arm vibration-induced pathology. This has been further refined and has become an important tool in occupational medicine. Thus, it is also important now to define the clinical stages of VAD in accordance with the appearance of the most common signs and symptoms. METHODS: We analyzed the files of 140 patients with VAD, paying close attention to the chronology of the clinical findings, the registry of eventual and on-the-job accidents, and the evaluation of disabilities. RESULTS: We have classified VAD in function of the time it took for 50% of the population to acquire the relevant sign or symptom. Stage I, mild signs (behavioral and mood associated with repeated infections of the respiratory tract, e.g., bronchitis); Stage II, moderate signs (depression and aggressiveness, pericardial thickening and other extracellular matrix changes, light to moderate hearing impairment, and discrete neurovascular disorders); Stage III, severe signs (myocardial infarction, stroke, malignancy, epilepsy, and suicide). CONCLUSION: This classification should be capable of assessing work fitness, and is a primary approach to a complex and multidisciplinary problem with implications in diagnosis, prevention and disability compensation within VAD.