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Individuals living or working in moldy buildings complain of a variety of health problems including pain, fatigue, increased anxiety, depression, and cognitive deficits. The ability of mold to cause such symptoms is controversial since no published research has examined the effects of controlled mold exposure on brain function or proposed a plausible mechanism of action. Patient symptoms following mold exposure are indistinguishable from those caused by innate immune activation following bacterial or viral exposure. We tested the hypothesis that repeated, quantified doses of both toxic and nontoxic mold stimuli would cause innate immune activation with concomitant neural effects and cognitive, emotional, and behavioral symptoms. We intranasally administered either 1) intact, toxic Stachybotrys spores; 2) extracted, nontoxic Stachybotrys spores; or 3) saline vehicle to mice. As predicted, intact spores increased interleukin-1β immunoreactivity in the hippocampus. Both spore types decreased neurogenesis and caused striking contextual memory deficits in young mice, while decreasing pain thresholds and enhancing auditory-cued memory in older mice. Nontoxic spores also increased anxiety-like behavior. Levels of hippocampal immune activation correlated with decreased neurogenesis, contextual memory deficits, and/or enhanced auditory-cued fear memory. Innate-immune activation may explain how both toxic mold and nontoxic mold skeletal elements caused cognitive and emotional dysfunction.

Most studies investigating cardiopulmonary resuscitation (CPR) interventions or functionality of mechanical CPR devices have been performed using porcine models. The purpose of this study was to identify differences between mechanical characteristics of the human and porcine chest during CPR.CPR data of 90 cardiac arrest patients was compared to data of 14 porcine from two animal studies. Chest stiffness k and viscosity mu were calculated from acceleration and pressure data recorded using a Laerdal Heartstart 4000SP defibrillator during CPR. K and mu were calculated at chest compression depths of 15, 30 and 50mm for three different time periods.At a depth of 15mm porcine chest stiffness was comparable to human chest stiffness at the beginning of resuscitation (4.8 vs. 4.5N/mm) and clearly lower after 200 chest compressions (2.9 vs. 4.5N/mm) (p0.05). At 30 and 50mm porcine chest stiffness was higher at the beginning and comparable to human chest stiffness after 200 chest compressions. After 200 chest compressions porcine chest viscosity was similar to human chest viscosity at 15mm (108 vs. 110Ns/m), higher for 30mm (240 vs. 188Ns/m) and clearly higher for 50mm chest compression depth (672 vs. 339Ns/m) (p0.05).In conclusion, human and porcine chest behave relatively similarly during CPR with respect to chest stiffness, but differences in chest viscosity at medium and deep chest compression depth should at least be kept in mind when extrapolating porcine results to humans.

Summary Background Ventilation with tidal volumes sufficient to raise the victim's chest is an integral part of guidelines for lay-rescuer basic life support, but optimal tidal volume, frequency and ratio to chest compressions are not known. Methods Adults with non-traumatic, out-of-hospital cardiac arrest, who were not successfully resuscitated following advanced life support by the staff of a physician-manned ambulance, were included. Advanced life support comprised tracheal intubation and mechanical ventilation with tidal volume of 700 ml and 100% oxygen, 12 times per min. An arterial blood sample was drawn at the end of the resuscitation attempt and analysed on the scene. After the victim was declared dead, basic life support was initiated with chest compressions and mouth-to-mask or mouth-to-tracheal tube ventilation (15:2), with volumes sufficient to make the chest rise. The tracheal tube was equipped with an impedance valve to avoid passive ventilation secondary to chest compressions. Arterial blood samples were drawn after 7–8 min of basic life support and analysed on the scene. Results Six men and two women, median (range) age 72 (32–86) years, were included in the study. Four of these received mouth-to-mask ventilation and four mouth-to-tracheal tube ventilation. Mean (S.D.) arterial blood carbon dioxide and oxygen tension during advanced life support were 6.4 (1.4) kPa and 22 (15) kPa, respectively. Similar values during basic life support were 9.6 (1.9) kPa and 8.5 (1.6) kPa, respectively, with no differences between the ventilation methods. Conclusion Ventilation during basic life support performed according to international guidelines (2000) resulted in arterial hypercapnia and hypoxia.

Summary Background Mortality among patients admitted to hospital after out-of-hospital cardiac arrest (OHCA) is high. Based on recent scientific evidence with a main goal of improving survival, we introduced and implemented a standardised post resuscitation protocol focusing on vital organ function including therapeutic hypothermia, percutaneous coronary intervention (PCI), control of haemodynamics, blood glucose, ventilation and seizures. Methods All patients with OHCA of cardiac aetiology admitted to the ICU from September 2003 to May 2005 (intervention period) were included in a prospective, observational study and compared to controls from February 1996 to February 1998. Results In the control period 15/58 (26%) survived to hospital discharge with a favourable neurological outcome versus 34 of 61 (56%) in the intervention period (OR 3.61, CI 1.66–7.84, p =0.001). All survivors with a favourable neurological outcome in both groups were still alive 1 year after discharge. Two patients from the control period were revascularised with thrombolytics versus 30 (49%) receiving PCI treatment in the intervention period (47 patients (77%) underwent cardiac angiography). Therapeutic hypothermia was not used in the control period, but 40 of 52 (77%) comatose patients received this treatment in the intervention period. Conclusions Discharge rate from hospital, neurological outcome and 1-year survival improved after standardisation of post resuscitation care. Based on a multivariate logistic analysis, hospital treatment in the intervention period was the most important independent predictor of survival.

Summary Background Adrenaline (epinephrine) is used during cardiopulmonary resuscitation (CPR) based on animal experiments without supportive clinical data. Clinically CPR was reported recently to have much poorer quality than expected from international guidelines and what is generally done in laboratory experiments. We have studied the haemodynamic effects of adrenaline during CPR with good laboratory quality and with quality simulating clinical findings and the feasibility of monitoring these effects through VF waveform analysis. Methods and results After 4min of cardiac arrest, followed by 4min of basic life support, 14 pigs were randomised to ClinicalCPR (intermittent manual chest compressions, compression-to-ventilation ratio 15:2, compression depth 30–38mm) or LabCPR (continuous mechanical chest compressions, 12 ventilations/min, compression depth 45mm). Adrenaline 0.02mg/kg was administered 30s thereafter. Plasma adrenaline concentration peaked earlier with LabCPR than with ClinicalCPR, median (range), 90 (30, 150) versus 150 (90, 270)s ( p =0.007), respectively. Coronary perfusion pressure (CPP) and cortical cerebral blood flow (CCBF) increased and femoral blood flow (FBF) decreased after adrenaline during LabCPR (mean differences (95% CI) CPP 17 (6, 29)mmHg ( p =0.01), FBF −5.0 (−8.8, −1.2) mlmin −1 ( p =0.02) and median difference CCBF 12% of baseline ( p =0.04)). There were no significant effects during ClinicalCPR (mean differences (95% CI) CPP 4.7 (−3.2, 13)mmHg ( p =0.2), FBF −0.2 (−4.6, 4.2)mlmin −1 ( p =0.9) and CCBF 3.6 (−1.8, 9.0)% of baseline ( p =0.15)). Slope VF waveform analysis reflected changes in CPP. Conclusion Adrenaline improved haemodynamics during laboratory quality CPR in pigs, but not with quality simulating clinically reported CPR performance.

Animals that rely on vocal communication must broadcast sound so that a perceptible signal is transmitted over an appropriate distance. We found that male blue-throated hummingbirds modified the amplitude of their vocalizations in response to both naturally occurring and experimenter-controlled changes in ambient noise levels. This phenomenon is known as the Lombard effect and may increase the efficiency of acoustic signalling. This study demonstrates the effect under natural field conditions and documents the first hummingbird species (Apodiformes: Trochilidae) to show this behaviour. We measured sound pressure levels (SPLs) of Serial Chip territorial advertisement calls across a natural range of ambient noise, primarily due to creeks within male territories. We found a significant correlation between the amplitude of Serial Chips and the amplitude of background noise. To test this relationship, we broadcast recordings of creek noise at high and low amplitudes while target individuals were producing Serial Chip vocalizations. We measured vocal SPLs before and during the playback. Individuals responded to changes in playback creek noise by changing the amplitude of Serial Chip production. We also measured transmission properties of Serial Chip calls through natural habitat to calculate the approximate amplitude of vocalizations at the position of the calling bird. We suggest that amplitude regulation of vocalizations contibutes to signal transmission distance along with the established relationships between singing behaviour, acoustic structure and habitat. Copyright 2003 Published by Elsevier Ltd on behalf of The Association for the Study of Animal Behaviour.

A recently developed Submerged Turret Loading concept (STL) for loading oil offshore is in use on several oil fields in the North Sea. A number of model-scale tests with the STL have been performed in the Hamburgische Schiffbau-Versuchsanstalt GmbH (HSVA) ice tank in Hamburg. The modelled ship had a conventional icebreaking bow and a length between perpendiculars of 235 m. The testing was performed at a scale of 1 : 36. The purpose of the tests was to study the feasibility of the STL concept in level ice, broken ice, and pressure ridges. The present paper describes the testing and results from the different tests. In level ice, 1.5 m full-scale ice thickness, 720 kPa flexural ice strength and 0.75 m/s speed, the average total force was 5868 kN with an average line tension in the front line of 2600 kN. The corresponding maximum loads were 8929 kN and 3507 kN. The mean value of the force peaks was 7285 kN and the standard deviation 932 kN. The measured forces (scaled) in level ice were therefore within the capacity of the present STL mooring system. Depending on the ridge consolidation, pressure ridges of the order produced for the present tests, may cause forces that exceed the capacity of the STL system. In broken ice, the average total forces did not exceed 2500 kN and the single mooring line loads were not above 1200 kN.

Our labs have developed a mouse model to study the neural basis of cognitive impairments following exposure to mold. Here, we compared the effects of mold exposure on individual microglial parameters across subregions of the dorsomedial hippocampus. Adult male C57Bl/6 mice were exposed to either intact spores (IN), extracted spores (EX), or saline vehicle (VEH). Extracted spores had their toxins removed and proteins denatured leaving the spore casing, thereby simulating spore components remaining after commercial mold abatement. Iba1 + cells were visualized using immunohistochemistry. Cell body contours in CA1 and CA2-3 (combined) were traced using Neurolucida (Microbrightfield). Standard Neurolucida contour parameters were compared across treatments and between hippocampal regions. In CA1, 2, 3 combined, cells were rounder and more compact in the IN group than in EX. EX cells had a more complex perimeter (form factor) than VEH or IN. Within the VEH group, cell bodies in CA1 were larger and more round than in CA2-3. There were no differences in any of the measured parameters between CA1 and CA2-3 in IN mice, and a different pattern of differences in parameters between CA1 and CA2-3 in EX mice. No differences in microglial density were found across hippocampal regions or treatments. In sum, both IN and EX mold treatment gives rise to characteristically different phenotype profiles of microglia in the hippocampus, specific to CA1 and CA2-3 subregions.

Approximately 40% of American buildings are moldy. Early studies found that neurologists could not differentiate between people who lived or worked in moldy buildings and patients with mild to moderate traumatic brain injury—they had the same neurological and cognitive deficits. Our laboratory developed a mouse model to determine how mold exposure might lead to cognitive dysfunction. One critical issue is whether exposure to any mold causes problems or only exposure to extremely toxic molds like Stachybotrys. We therefore quantified the effects of exposure to (1) intact Stachybotrys spores (IN) containing a variety of toxins, volatile organic compounds and proteinases, (2) Stachybotrys spores extracted twice with ethanol (EX) to remove toxins and denature proteins, or (3) the nonpyrogenic saline vehicle (VEH). Mice were nasally instilled 3X per week. After 5 weeks, EX mice performed significantly worse in finding the hidden platform in the Morris water maze (MWM) than VEH or IN mice, taking longer to find the platform and using longer paths. Surprisingly. IN mice showed evidence of lesser memory impairment. MWM performance in EX and IN mice was inversely correlated with numbers of interleukin-1 β cells in dorsomedial CA1 as well as with weight gain over the first 3 weeks of treatment. Clearly, exposure to just the mold skeleton is sufficient to cause brain inflammation and cognitive deficits, suggesting exposure to any mold could be problematic.

Exposure to indoor mold causes deficits in learning and memory, however the neural mechanisms for these effects have not been established. Earlier work from our labs using a mouse model determined that exposure to the mold Stachybotrys resulted in central inflammation, decreased survival of newly formed hippocampal neurons, and impaired hippocampal-dependent memory. Here we treated mold-exposed animals with a doxycycline diet (DD) to determine whether antibiotic treatment would mitigate the effects of mold exposure. Adult male C57Bl/6 mice were given intact mold spores (IN) intranasally or saline vehicle (VEH) 3x/week for 4 weeks. Half of the IN and VEH animals received doxycycline in their diet (DD). All mice were injected with BrdU 31–37 days prior to sacrifice. We quantified BrdU+/NeuN+ new neurons and iba1-expressing cells within the dorsomedial dentate gyrus. The latter were characterized as ramified, primed, ameboid, rod-like, migratory or monocyte-like. DD increased Iba1+ cells overall, and also ramified cells specifically, in both VEH and IN groups. IN increased monocyte-like cells, which were not attenuated by DD. Interestingly, numbers of migratory microglial cells were positively correlated with numbers of mature new neurons in the subgranular zone across treatment groups, suggesting a potential neuroprotective role for this microglial phenotype. In sum, DD increased numbers of microglial cells in the dentate gyrus but did not prevent infiltration of monocyte-like cells.

Exposure to mold in water-damaged buildings can have severe adverse effects on human health. Despite evidence that mold exposure causes increased anxiety, depression, chronic fatigue, pain, and cognitive problems, no animal research has been published examining how mold exposure causes these problems. We examined the effects of exposing mice to spores of Stachybotrys chartarum, probably the most studied of the damp-building molds. Mice were exposed to either intact Stachybotrys spores, containing a variety of potent toxins and proteinases (IN), to spores extracted twice with alcohol to remove spore contents (EX), or to saline vehicle (VEH). Both types of spores cause significant memory deficits on a contextual memory task. Mice treated with extracted spores show significantly higher levels of anxiety, while mice treated with intact spores are more fearful of an auditory tone previously paired with a mild footshock. Spore inhalation significantly increased numbers of interleukin-1β-immunoreactive cells in the dorsomedial hippocampus In IN males, with EX males being intermediate between IN and VEH males. EX treatment significantly decreased numbers of immature new neurons as quantified by doublecortin, while IN treatment significantly reduced numbers of mature new neurons as quantified by double labeling with BrdU and NeuN. Our data suggest that respiratory exposure to any mold, not just the particularly toxic ones like Stachybotrys, may be capable of causing brain inflammation, cognitive deficits, and emotional problems.

Mold exposure can cause cognitive impairment. We recently developed a mouse model to determine mechanisms leading to impaired cognition. We found that repeated exposure to the mold Stachybotrys caused deficits in hippocampal memory. We hypothesized that these effects are mediated, in part, by increased inflammation and decreased survival of new neurons. Adult mice were instilled intranasally with low doses of intact mold spores, extracted spore skeletons, or saline vehicle (3x wk/ 6 wks). Extracted spores had toxins removed and proteins denatured. Brains were processed to label the pro-inflammatory cytokine interleukin-1β (Il-1β), immature new neurons (doublecortin) or mature new neurons (bromodeoxyuridine/NeuN) and quantified throughout the dorsomedial dentate gyrus. Earlier, we showed that exposure to both intact and extracted spores resulted in the same memory deficits. Here we found significantly fewer mature new neurons following exposure to intact spores, and fewer young neurons in mice treated with extracted spores. This suggests that intact and extracted spores may induce the same cognitive impairment via different mechanisms. Interestingly, we also found an inverse correlation between numbers of cells expressing Il-1β and mature new neurons, and a positive correlation between cells expressing IL-1β and numbers of young neurons. We suggest that decreased survival of older neurons associated with inflammation results in a compensatory increase in younger neurons. However the increase is insufficient to overcome overall decreased numbers of mature new neurons.

Obesity is clearly a risk factor for increased basal inflammation and increased inflammatory responses to immune challenge. However, even weight variation within the normal range or in food-restricted animals is correlated with the immune response to a pathogen challenge and changes in behavior. We discovered that mice’s adverse responses to mold exposure were strongly correlated with body weight. In fact, small variations in body weight were better predictors of inflammation and/or cognitive effects than spore dose. Male C57Bl/6 mice were randomly assigned to treatment groups according to a stratified block design controlling for initial weight. Mice were nasally instilled with (1) intact Stachybotrys spores, (2) extracted spores that had their toxins removed and proteins denatured, or (3) saline vehicle three times per week. Their behavior was tested after three weeks of treatment, and the animals sacrificed and hippocampal tissue analyzed after six weeks. Weight did not differ across groups at any point in the experiment. However, the more the animals weighed, the higher the numbers of amoeboid microglia in the hippocampus, the greater the memory deficits on a contextual fear task, the higher the anxiety as measured on the elevated plus maze and the more fearful the animals were of the auditory cue that had been paired with one mild footshock. Clearly, weight within the normal range is a crucial variable in inflammatory responses leading to cognitive changes.

Multiple balloon recordings of bremsstrahlung X-rays supported by recordings of cosmic noise absorption have been used to study in detail energetic (≥30 keV) electron precipitation events occurring near local midnight at the onset of the expansion phase of magnetospheric substorms. This type of precipitation occurs during the first 5–10 min after bay onset and can usually be distinguished from the subsequent bay-associated precipitation by its characteristic time structure, variation in energy spectrum, and higher intensities. During this same interval, the poleward border of the precipitation region moves rapidly towards higher latitudes with speeds of typically 1–2 km/s, whereas the equatorward border seems to move slowly towards lower latitudes. The northward expansion starts just poleward of the lowest latitude reached during the slow equatorward motion of the preceding growth-phase precipitation. The previous narrow precipitation region may thus expand to as much as 10° of invariant latitude within a few minutes. Within the expanding region there are additional intrinsic temporal variations. As the flux of precipitating electrons tends to be most intense and most energetic near the poleward border, recordings made northward of the latitude where the poleward motion started tend to give the appearance of an impulsive precipitation event. The bay-onset precipitation starts abruptly at the onset of Pi 2 magnetic pulsations. Associated with these pulsations there are modulations of the flux of precipitating electrons. An intensified westward electrojet appears to have its center in the equatorward part of the precipitation region. It is suggested that the poleward expansion is associated with the expansion of the plasma sheet earthward of a newly formed X-type neutral line, and is caused by a sudden enhancement of field-line re-connection across the neutral sheet. The intense, more energetic electron precipitation at the poleward border of the precipitation region then takes place along the outer border of the expanding plasma sheet.

Simultaneous balloon recordings of auroral-zone X-rays from precipitating electrons, covering a range of L -values from ≈5 to ≈7.5, are presented. The precipitation event was observed in the early morning sector (from about 0200 to 0500 local magnetic time), and was associated with a negative magnetic bay. Before the bay, precipitation associated with the growth phase of the substorm was observed at high L -values. After bay onset, precipitation was observed over the whole range of L -values covered, but with a delayed onset in the southern part of the precipitation region as compared with the onset of cosmic noise absorption in the local midnight sector. At high L -values the X-ray flux was completely unstructured and drizzle-like, both before and after bay onset. At low L -values, where precipitation occurred only after bay onset, the event was splash-like with X-ray bursts of typically 4–6 sec duration apparently rising out of the cosmic-ray background. The precipitation bursts had spatial extensions of 300–400 km. They were accompanied by weak magnetic impulses which were, both temporally and spatially, closely related to the X-ray bursts. The unstructured precipitation at high L -values was apparently associated with and extending along the auroral electrojet, presumably representing freshly accelerated particles. The highly structured and burst-like precipitation to the south seems to have come from a cloud of electrons drifting out from the acceleration region, from which wave-particle instabilities or some other mechanism caused electrons to be precipitated.

Unweathered Monterey kerogens from surface samples and wells in the Santa Barbara area and the Salinas Basin (approximately 125 miles apart), are oil-prone good to excellent potential oil source rocks deposited under marine anoxic to suboxic conditions. The kerogens in the surface samples are somewhat similar when viewed through the microscope and the differences result from the depositional conditions (anoxic vs suboxic) and the original organic matter that formed the amorphinite (alginite vs exinite). The bitumens extracted from these samples have similar carbon isotope values and gas chromatography fingerprints. In the Santa Barbara area, mudstones from the lower calcareous facies of the Monterey Formation contain greater than 90% fluorescent marine, Amorphinite II kerogen, that is oil prone (Type II and mixed Type II and III) based on Rock-Eval and TOC analysis. In the Salinas Basin, kerogens from the calcerous Sandholdt Member of the Monterey Formation (equivalent to the lower calcareous facies) also contain greater than 90% amorphous, highly oil-prone Amorphinite II. The upper siliceous Monterey Formation in the Santa Barbara area also contains large amounts of oil-prone, Amorphinite II and is compared to the weathered siliceous Hames Member in the Salinas Basin that contains a large amount of Alginite. The kerogens in the lower calcerous facies in both areas are thermally immature but contain solid bitumen and/or oil droplets in the residues at low levels of vitrinite reflectance and TAI (mean R o values from 0.3 to 0.4% and TAI values from 2.2 to 2.5).

Multiple balloon recordings of bremsstrahlung X-rays from a large scale auroral-zone electron precipitation event are presented. Additional riometer recordings show that it extended from noon, via dusk, to midnight. The X-ray observations show electron precipitation over a range of L -values from ∼− 5.5 to 7.5. This was briefly interrupted during a negative sudden impulse in the geomagnetic field. A close similarity between variations in the X-ray fluxes and locally recorded variations in the geomagnetic field was observed. Magnetic records from around the auroral zone suggest that the precipitation was related to an asymmetric magnetospheric convection system.

The morphology of energetic (≥30 keV) electron precipitation during the growth phase of magnetospheric substorms has been investigated using measurements of auroral-zone bremsstrahlung X-rays obtained from multiple balloon flights and supplementing riometer recordings. Growth-phase precipitation typically starts about one hour before the onset of a negative magnetic bay and occurs in a limited region parallel to the auroral oval around local midnight. The precipitation is first observed in the northern part of the auroral zone and moves southwards with a speed of 5–10 km/min. To the north this precipitation therefore ceases well before bay onset whereas a continuous transition from ‘prebay’ precipitation to bay-associated precipitation takes place in the south. A decrease in the intensity or at least a levelling off may occur some minutes before bay onset. The southward movement of the precipitation region is associated with a similar movement of a weak ionospheric current system. The events studied were all associated with a southward-pointing interplanetary magnetic field and with growth-phase conditions in the magnetotail. It is suggested that growth-phase precipitation originates from the ‘horns’ of the plasma sheet. The equatorward motion of the precipitation is then a consequence of an expansion of the polar cap, a thinning of the plasma sheet, and an equatorward motion of its inner edge. It is also suggested that this precipitation provides a stabilization of the outer boundaries of the plasma sheet by restricting the ionospheric mobility of the bordering field lines through enhanced conductivity.

Changes in structures within bouncing bursts of energetic (≳30 keV) electrons due to velocity dispersion have been estimated. Theoretical calculations show that power spectra of electron intensity fluctuations at ionospheric heights are increasingly damped with increasing frequencies relative to their source spectra. This damping depends strongly on the distance travelled by the electron burst from the burst source region to the ionosphere, but is only weakly dependent on the electron energy spectra. A similar dependence is also found for the ratio between power spectra of electron fluxes above two different threshold energies. These calculations are compared with the observed relative damping rates in power spectra of auroral-zone X-ray microbursts which are caused by bursts of precipitating electrons. On the basis of this comparison it is inferred that the source region of the individual electron bursts is located between the ionosphere and the equator, but probably well off the equatorial plane. The typical fine-structures within X-ray microbursts with frequencies above ~2 Hz are apparently generated quite close to the ionosphere.

Balloon recordings of bremsstrahlung X-raya from precipitating electrons are presented, showing impulsive X-ray events just at the onset of bay activity as well as weaker and smoother electron precipitation before the bay, the latter apparently being connected with a growth phase of the same substorm. The pre-bay events are generally very smoothly varying events, but show modulation effects associated with the occurrence of irregular magnetic pulsations. The impulsive precipitation events start very abruptly together with Pi 2 magnetic pulsations at bay onset, and also show modulation effects, so that maxima in the X-ray flux tend to accompany maxima in the H -component at auroral-zone stations. These X-ray pulsations have a shorter period than the simultaneous mid-latitude Pi 2, which we take to indicate that the impulsive precipitation events occur on field lines close to the inner edge of the neutral sheet.

The effect of an interaction Hamiltonian linear in the phonon field and quadratic in the spin operators on a system of noninteracting spin waves and phonons for an ideal Heisenberg ferromagnet is examined by using the techniques of quantum field theory. Assuming the coupling to be weak, a perturbation expansion is performed, and the renormalized spin wave and phonon energies are calculated to lowest order, together with the lifetimes of the individual excitation modes. The calculations are performed separately for two different approximations for the spin system. The random phase approximation (1) is used to study the behavior of the system near the Curie temperature, and the Holstein-Primakoff approximation (2) is used at low temperatures. The interaction leads to a shift in the Curie temperature, Tc, but the behavior of the magnetization, σ, (calculated in RPA) in the neighborhood of the Curie temperature is virtually unchanged. At low temperatures, in addition to a renormalization of the coefficient of the Bloch T 3 2 term (3), a T4 term is obtained in the magnetization which is entirely due to the interaction. The sound velocity is renormalized by the interaction; the change in the sound velocity vanishes at T = 0 and also for T = Tc in the absence of an external magnetic field. In the neighborhood of the Curie temperature the phonon spectrum is found to have a term linear in σ. Because dσ dT is large (∞ in RPA) at Tc, the phonon contribution to thermodynamic quantities involving ( dω dT )(q, T) like the specific heat, will be peaked at the Curie point. Finally, an expression for the thermal expansion coefficient of the lattice is derived which, in addition to the usual term proportional to the phonon contribution to the specific heat, is found to have a term proportional to the specific heat of the spin system. Therefore, the thermal expansion coefficient will have a discontinuity at Tc, as expected in a phase transition of the second kind. At low temperatures it is porportional to T 3 2 , the spin contribution again being dominant.

The contribution of the electron-phonon interaction to the effective mass, the superconducting transition temperature and the d.c. resistivity has been calculated for aluminium using two different effective potentials. The conduction electrons were described by two orthogonalized plane waves, and the distortion of the Fermi surface near the zone boundaries was taken into account in an approximate way. The experimental phonon dispersion curves were used. For the potential constructed by Ashcroft agreement with experiment to better than 10% was found for the effective mass and the parameter NV , determining the transition temperature, while the resistivity at 300°K was too low by about 25%. The pseudopotential constructed by Harrison gave too large values for all three quantities, by as much as 45% for the resistivity at 300°K. Using the Ashcroft potential, the resistivity was calculated for temperatures from 10°K to 900°K. In this calculation it was important to include the temperature dependence of the phonon spectrum.

Based on recent X-ray data, it is suggested that the phase transition in Gd 2 (MoO 4 ) 3 is a structural transition driven by a soft q ≠ 0 mode. A tentative model to account for the elastic and ferroelectric properties is presented.