Polarized phonons carry angular momentum in ultrafast demagnetization.

Magnetic phenomena are ubiquitous in nature and indispensable for modern science and technology, but it is notoriously difficult to change the magnetic order of a material in a rapid way. However, if a thin nickel film is subjected to ultrashort laser pulses, it loses its magnetic order almost completely within femtosecond timescales1. This phenomenon is widespread2-7 and offers opportunities for rapid information processing8-11 or ultrafast spintronics at frequencies approaching those of light8,9,12. Consequently, the physics of ultrafast demagnetization is central to modern materials research1-7,13-28, but a crucial question has remained elusive: if a material loses its magnetization within mere femtoseconds, where is the missing angular momentum in such a short time? Here we use ultrafast electron diffraction to reveal in nickel an almost instantaneous, long-lasting, non-equilibrium population of anisotropic high-frequency phonons that appear within 150-750 fs. The anisotropy plane is perpendicular to the direction of the initial magnetization and the atomic oscillation amplitude is 2 pm. We explain these observations by means of circularly polarized phonons that quickly absorb the angular momentum of the spin system before macroscopic sample rotation. The time that is needed for demagnetization is related to the time it takes to accelerate the atoms. These results provide an atomistic picture of the Einstein-de Haas effect and signify the general importance of polarized phonons for non-equilibrium dynamics and phase transitions.

[MEDCARE for People in Eritrea : A report on 9 years' help through self-help]. / MEDCARE for People in Eritrea : Ein Bericht über 9 Jahre Hilfe zur Selbsthilfe.

The current article is an experience report on the establishment of an ENT clinic in Asmara/Eritrea and the organization of regular work stays for the further education of local colleagues. Objectives of the project are content and structural support for self-help and thus achievement of sustainable development aid, which benefits both the medical development of the country and the care of the local patients.

Antimicrobial Activity of Actinobacteria Isolated From the Guts of Subterranean Termites.

Subterranean termites need to minimize potentially pathogenic and competitive fungi in their environment in order to maintain colony health. We examined the ability of Actinobacteria isolated from termite guts in suppressing microorganisms commonly encountered in a subterranean environment. Guts from two subterranean termite species, Reticulitermes flavipes (Kollar) and Reticulitermes tibialis Banks, were extracted and plated on selective chitin media. A total of 38 Actinobacteria isolates were selected for in vitro growth inhibition assays. Target microbes included three strains of Serratia marcescens Bizio, two mold fungi (Trichoderma sp. and Metarhizium sp.), a yeast fungus (Candida albicans (C.P. Robin) Berkhout), and four basidiomycete fungi (Gloeophyllum trabeum (Persoon) Murrill, Tyromyces palustris (Berkeley & M.A. Curtis) Murrill, Irpex lacteus (Fries) Fries, and Trametes versicolor (L.) Lloyd). Results showed both broad and narrow ranges of antimicrobial activity against the mold fungi, yeast fungus, and S. marcescens isolates by the Actinobacteria selected. This suggests that termite gut-associated Actinobacteria produce secondary antimicrobial compounds that may be important for pathogen inhibition in termites. Basidiomycete fungi were strongly inhibited by the selected Actinobacteria isolates, with G. trabeum and T. versicolor being most inhibited, followed by I. lacteus and T. palustris The degree of inhibition was correlated with shifts in pH caused by the Actinobacteria. Nearly all Actinobacteria isolates raised pH of the growth medium to basic levels (i.e. pH ∼8.0-9.5). We summarize antimicrobial activity of these termite gut-associated Actinobacteria and examine the implications of these pH shifts.

[Mycobacterium ulcerans disease (Buruli ulcer) in Gabon: 2005-2011]. / L'infection à Mycobacterium ulcerans (ulcère de Buruli) au Gabon de 2005 à 2011.

The first cases of Buruli ulcer (BU) in Gabon were described in the 1960s. Between 2005 and 2011, 301 clinically suspected cases of BU were found in all nine provinces of Gabon, and their lesions sampled for microbiological confirmation. Polymerase chain reaction (PCR) found 120 (39.9%) of these lesions positive and 181 (60.1%) negative for Mycobacterium ulcerans. The confirmed cases came mainly from the province of Moyen-Ogooué, particularly from localities along the Ogooué River (n=117; 52.5% of the samples in this province were PCR-positive). The detection rates per 100,000 inhabitants in this province ranged from 94.7 cases in 2005 to 28 in 2007, after an absence of active case-finding in 2006. The final three PCR-positive cases were found in the province of Estuaire. The characteristics of the confirmed BU patients (that is, PCR-positive) were identical to those described in other African countries: most patients were younger than 15 years old, and most lesions were found on both the upper and lower limbs. The group of suspected cases (PCR-negative) differed from the PCR-positive group for patient age (most patients were aged 15 to 49 years), lesion location (more frequently on the lower limbs), and ulceration (more frequent in the suspected cases). Some PCR-negative patients probably had other diseases; this underlines the importance of the differential diagnosis of BU. The cure rate of PCR(-)confirmed cases in our study was 88%; treatment was the antibiotic combination recommended by the World Health Organization (WHO). Our study demonstrates that BU is endemic in Gabon and is a public health problem there. Patients consult late with often extensive lesions. Awareness campaigns should be pursued to ensure earlier treatment of patients. The influence of HIV on BU in Gabon also deserves particular attention.

[Methemoglobin intoxication by prilocaine in EMLA. Accidental intoxication of an infant with scald injuries]. / Methämoglobinintoxikation durch Prilocain in EMLA. Akzidentelle Intoxikation bei einem Kleinkind mit Verbrühungen.

The case of an infant who had received EMLA(R) for local pain therapy after scalding to 5% of the body surface with boiling water is reported. Due to the application of EMLA(R) on the injured skin and exceeding the recommended doses of prilocaine and lidocaine the child developed symptomatic methemoglobinemia. During surgical wound dressing the boy showed cyanosis, decreased peripheral oxygen saturation and potentially suffered a general seizure. With a symptomatic therapy including mechanical ventilation and anticonvulsive drugs the methemoglobinemia normalized within 9 h. The child recovered without any neurological impairment after wound treatment was completed.

Associations between the Holden Psychological Screening Inventory and the Personality Assessment Screener in a nonclinical sample.

Associations between two screening inventories of psychopathology were investigated using a sample of 156 first-year undergraduates. Analyses supported the reliability and validity of all Holden Psychological Screening Inventory scales, but only of some of the Personality Assessment Screener scales. Orthogonal dimensions of Depression, General Distress, and Antisocial Tendencies represented the common latent structure of the two inventories.

Criterion validity of the Holden Psychological Screening Inventory Social Symptomatology scale in a prison sample.

The 36-item, self-report Holden Psychological Screening Inventory (HPSI; R. R. Holden, 1996) and the Psychopathy Checklist--Revised (PCL-R; R. D. Hare, 1991) were administered to 214 male, adult prison inmates in Canadian federal correctional facilities. The 12-item HPSI Social Symptomatology scale, a measure of antisocial behavior, demonstrated a large effect size in significantly differentiating between PCL-R-identified psychopaths and nonpsychopaths. HPSI scales not theoretically related to psychopathic behavior showed no such significant effects. Findings are interpreted as supporting the criterion validity of the Social Symptomatology scale and suggest that this brief, self-report screen has research and clinical merit.

Reversion of human glioblastoma malignancy by U1 small nuclear RNA/ribozyme targeting of scatter factor/hepatocyte growth factor and c-met expression.

BACKGROUND: Expression of scatter factor (SF), also known as hepatocyte growth factor (HGF), and its receptor, c-met, is often associated with malignant progression of human tumors, including gliomas. Overexpression of SF/HGF in experimental gliomas enhances tumorigenicity and tumor-associated angiogenesis (i.e., growth of new blood vessels). However, the role of endogenous SF/HGF or c-met expression in the malignant progression of gliomas has not been examined directly. In this study, we tested the hypothesis that human glioblastomas can be SF/HGF-c-met dependent and that a reduction in endogenous SF/HGF or c-met expression can lead to inhibition of tumor growth and tumorigenicity. METHODS: Expression of the SF/HGF and c-met genes was inhibited by transfecting glioblastoma cells with chimeric transgenes consisting of U1 small nuclear RNA, a hammerhead ribozyme, and antisense sequences. The effects of reduced SF/HGF and c-met expression on 1) SF/HGF-dependent induction of immediate early genes (c-fos and c-jun), indicative of signal transduction; 2) anchorage-independent colony formation (clonogenicity), an in vitro correlate of solid tumor malignancy; and 3) intracranial tumor formation in immunodeficient mice were quantified. Statistical tests were two-sided. RESULTS: Introduction of the transgenes into glioblastoma cells reduced expression of the SF/HGF and c-met genes to as little as 2% of control cell levels. Reduction in c-met expression specifically inhibited SF/HGF-dependent signal transduction (P<.01). Inhibition of SF/HGF or c-met expression in glioblastoma cells possessing an SF/HGF-c-met autocrine loop reduced tumor cell clonogenicity (P =.005 for SF/HGF and P=.009 for c-met) and substantially inhibited tumorigenicity (P<.0001) and tumor growth in vivo (P<.0001). CONCLUSIONS: To our knowledge, this is the first successful inhibition of SF/HGF and c-met expression in a tumor model directly demonstrating a role for endogenous SF/HGF and c-met in human glioblastoma. Our results suggest that targeting the SF/HGF-c-met signaling pathway may be an important approach in controlling tumor progression.

Scatter factor/hepatocyte growth factor gene transfer increases rat blood-glioma barrier permeability.

Malignant gliomas are associated with a dysfunctional blood-tumor barrier (BTB) that causes substantial morbidity. Scatter factor/hepatocyte growth factor (SF/HGF) is a multifunctional growth factor that correlates with glioma malignancy and has several biological properties that suggest a role in enhancing blood-glioma barrier permeability. In this study, we examined the effects of glioma cell SF/HGF expression on BTB permeability to horseradish peroxidase (HRP). Fischer 344 rats bearing intrastriatal 9L tumors engineered to secrete SF/HGF (9L-SF) and SF/HGF-negative control tumors (9L-neo) received intracardiac injections of HRP and were rapidly decapitated. Densitometric analysis of brain sections reacted with diaminobenzidine showed significantly greater extravascular HRP surrounding SF/HGF-secreting tumors than 9L-neo tumors of comparable size (p<0.05). HRP enzymatic activity associated with striata containing SF/HGF-expressing tumors was 1. 6-fold greater than that of striata containing control tumors (p<0. 05). Northern analysis showed that expression of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) did not differ between 9L-neo and 9L-SF tumors. These data demonstrate that SF/HGF expression by intracerebral glial tumors can enhance BTB permeability independent of changes in VEGF/VPF expression.

IL-10 gene transfer to intracranial 9L glioma: tumor inhibition and cooperation with IL-2.

This study examines the effects of interleukin-10 (IL-10) and combination IL-10 + IL-2 gene transfer on experimental brain tumor growth in vivo. 9L gliosarcoma cells were engineered to stably express murine IL-10 (9L-IL-10 cells) and implanted subcutaneously or to the caudate/putamen of syngeneic rats. The growth of tumors expressing IL-10 was substantially reduced compared to that of control tumors (p < 0.05). Intracranial tumors expressing IL-10 and IL-2 were established by co-implanting 9L-IL-10 cells with endothelial cells engineered to express IL-2. At 14 days post-implantation, tumors expressing IL-10 + IL-2 were 99% smaller than control-transfected tumors (p < 0.0001). This extent of anti-tumor effect could not be achieved by expression of IL-10 or IL-2 alone within tumors. Neither IL-10 nor a combination of IL-10 + IL-2 gene delivery inhibited tumor growth in severe combined immunodeficient (SCID-Beige) mice (p > 0.05). Immunohistochemical analysis revealed that IL-10 + IL-2 gene delivery markedly increased T-cell infiltration within the striatum ipsilateral to tumor cell implantation. These findings establish that IL-10 expression, particularly in combination with IL-2 expression, can have significant immune-dependent anti-tumor actions within intracranial gliomas.

Environmental influences on psychological restoration.

Research on psychological restoration and restorative environments is a needed complement to work on stress and environmental stressors. Two laboratory experiments tested the utility of two restorative environments theories, one concerned with directed attention capacity renewal and the other with stress reduction and associated changes in emotion. Various strategies were employed to distinguish restorative effects from other effects, to limit the role of arousal reduction in attentional restoration, and to begin mapping the time course for the emergence of outcomes. Both experiments tested for differential emotional and performance effects as a function of photographic environmental simulation (natural or urban environment). Across the experiments the natural environment simulation engendered generally more positive emotional self-reports. That consistent performance effects were not found in either study suggests that attentional restoration as reflected in performance is a more time-intensive process.

Altered expression of microtubule-associated proteins in cat trochlear motoneurons after peripheral and central lesions of the trochlear nerve.

Neurons lesioned in the peripheral nervous system (PNS) generally regenerate and survive, while neurons lesioned in the central nervous system (CNS) do not regenerate and often die. Investigators have traditionally compared the neuronal responses to PNS and CNS lesions in two separate populations of neurons. In this study, we compared the effects of PNS and CNS lesions on the expression of cytoskeletal proteins in a single neuronal population, the trochlear motoneurons of the cat. The trochlear nerve was lesioned either unilaterally in the PNS or bilaterally in the CNS (within the anterior medullary velum), and animals were allowed to survive 1, 2, or 4 weeks. Brain sections were reacted immunocytochemically using antibodies against microtubule -associated protein-2 (MAP-2) and a phosphorylated isoform of MAP1B, termed MAP1B-P. MAP-2 immunoreactivity (IR) was significantly decreased in the CNS-lesioned trochlear nucleus, compared to the lesioned and the unlesioned trochlear nucleus of PNS-lesioned animals. MAP1B-P IR was significantly increased in PNS- and CNS- lesioned trochlear axons, compared to axons in the unlesioned trochlear nerve of PNS-lesioned animals, and appeared in a small percentage of PNS- and CNS-lesioned cell bodies. These results support the growing body of evidence that MPA-2 can serve as a marker for cells that will eventually die following neuronal insult. The increased immunostaining of MAP1B-P in lesioned axons and its appearance in lesioned cell bodies are characteristic of the immature CNS and may reflect an initial recapitulation of early development, when the levels of this protein are high.

The effects of immunolesions of nerve growth factor-receptive neurons by 192 IgG-saporin on sleep.

Low-affinity nerve growth factor (NGF) receptors are present on the cholinergic neurons of the basal forebrain. We studied the effects of 192 IgG-saporin, a specific immunotoxin for the NGF receptor-positive, cholinergic basal forebrain neurons, on sleep, the power spectrum of the electroencephalogram (EEG), and body temperature. After 3 d baseline recordings, 12 male rats were injected intracerebroventricularly with 4 micrograms 192 IgG-saporin. EEG, motor activity, and brain temperature were recorded for 23 h on the first, third, fifth, and seventh day after the treatment. 192 IgG-saporin did not affect the total daily amounts but altered the circadian distribution of sleep. On days 1 and 3 after the injection of the immunotoxin, the amount of non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased during the dark period, whereas during the light both NREMS and REMS decreased. On day 5, these changes were less pronounced and sleep completely returned to the baseline by day 7. The EEG was suppressed in each frequency band and each vigilance state, and, in contrast to sleep, these changes in EEG persisted for 7 days. Brain temperature was decreased from day 3. These results suggest that NGF receptor-positive, cholinergic basal forebrain neurons are not necessary for the maintenance of total sleep time but contribute to the generation of normal EEG and the maintenance of brain temperature.

Couverture vaccinale 1994 dans l'aire de sante de Soboum-Zone Nylon (Douala; Cameroun)

L'enquete de couverture vaccinale realisee en 1994 dans l'aire de sante de Soboum (Zone Nylon) a montre des resultats mediocres; tres eloignes des objectifs que l'OMS a fixes pour 1995. Manque d'information; manque de motivation et obstacles a la vaccination sont les principaux responsables de cette situation. L'information sanitaire et la participation communautaire doivent etre redynamisees; ainsi que la formation du personnel et le monitorage du programme

192 IgG-saporin. 2. Neuropathology in the rat brain.

We have previously shown that an immunotoxin (IT) directed against the p75 component of the nerve growth factor receptor (NGFr) selectively abolished cholinergic neurons in the basal forebrain of the rat following intraventricular administration. We now report the neuropathological responses in the rat brain to the IT, with particular emphasis on the cholinergic basal forebrain (CBF) and other known p75NGFr-positive brain regions. Animals received intraventricular injections of IT and were allowed to survive for various times. Sections through the entire brain were evaluated using (1) hematoxylin and eosin; (2) glial fibrillary acidic protein immunohistochemistry; and (3) Griffonia simplicifolia lectin histochemistry. The only clearly degenerating cells following IT treatment were located in the CBF or in the Purkinje cell layer of the cerebellum. A marked microglial response was demonstrated that was tightly linked both topographically and temporally to the loss of neurons in these areas. The astroglial response was mild in the same regions in which the microglial response was obvious. The other areas of rat brain including the terminal fields of CBF projections showed no consistent reactive cellular responses in IT-treated animals. This study extends and corroborates previous work indicating specificity of IT, demonstrates active neuronal degeneration by conventional pathological methods for the first time, and illustrates the unexpected and novel finding that the predominant pathological response to the IT-induced loss of neurons is microglial. Both the high degree of specificity and the distinctive glial response distinguish the IT model from other experimental models of CBF neurodegeneration.

192 IgG-saporin causes a major loss of synaptic content in rat olfactory bulb.

An immunotoxin composed of a monoclonal antibody that recognizes the p75 nerve growth factor (NGF) receptor disulfide-linked to the ribosome-inactivating protein saporin selectively eliminates p75-expressing cholinergic neurons in the basal forebrain, while sparing other neurons in the forebrain, both cholinergic and noncholinergic. We now report the effect that intraventricular administration of this immunotoxin has on the synaptic content of the olfactory bulb, one of the major terminal fields of the cholinergic basal forebrain system. Control substances or immunotoxin were given to rats followed by a 2-week survival. Unilateral transection of the olfactory tract and peduncle was also studied. Both qualitative and quantitative evaluation of olfactory bulbs processed for synaptophysin immunohistochemistry indicated dramatic loss of synapses in the four regions of neuropil evaluated (glomeruli, outer and inner halves of the external plexiform layer, and internal plexiform layer) compared with the administration of control substances. Surgical transection of the bulb produced a visually similar decrement, but quantitative studies showed synaptic loss to be consistently greater following tract transection. The effects of these two insults on the glial response were remarkably different. Transection produced an obvious hyperplasia and hypertrophy of both astrocyte and microglial elements, while immunotoxin produced small, almost undetectable reactions by these two cell types. The results in the glomeruli strongly suggest an effect of the immunotoxin on either periglomerular cells or olfactory nerve terminals, whether directly by NGF receptor (+) structures or by trans-synaptic mechanisms. We conclude that the immunotoxin produces a specific and large loss of synapses that does not produce much glial response.

192 IgG-saporin: I. Specific lethality for cholinergic neurons in the basal forebrain of the rat.

An immunotoxin (IT) composed of a monoclonal antibody to the nerve growth factor (NGF) receptor, 192 IgG, chemically linked to saporin, 192 IgG-saporin, was shown to selectively reduce forebrain choline acetyltransferase (ChAT) activity in the rat brain following intraventricular administration. In order to determine if the IT was killing NGF receptor-positive neurons in the CBF (rather than simply suppressing the cholinergic phenotype in these cells), a population of neurons in the nucleus basalis magnocellularis (NBM) was prelabeled by an intracortical injection of the neurotracer Fluoro-Gold (FG) 1 week before intraventricular injections of IT or control substances (reduced IT or phosphate-buffered saline). We found that there were very few double-labeled (i.e. FG-labeled and ChAT-positive) neurons remaining in the NBM of IT-treated animals. The absolute number of FG-labeled neurons in the NBM of IT-treated animals was reduced by a number similar to the counts of double-labeled neurons in the NBM of control animals. Our conclusion is that the IT is preferentially lethal to cholinergic neurons in the NBM. Due to its ability to selectively kill cholinergic neurons in the CBF and concomitantly spare noncholinergic neurons with similar morphology and projections, 192 IgG-saporin can be used to produce a selective model of CBF deficit in the rat.

Specificity of 192 IgG-saporin for NGF receptor-positive cholinergic basal forebrain neurons in the rat.

A monoclonal antibody to the rat nerve growth factor (NGF) receptor, 192 IgG, accumulates bilaterally and specifically in cholinergic basal forebrain (CBF) cells following intraventricular injection. An immunotoxin composed of 192 IgG linked to saporin (192 IgG-saporin) has been shown to destroy cholinergic neurons in the basal forebrain. We sought to determine if intraventricular 192 IgG-saporin affected choline acetyltransferase (ChAT) enzyme activity in the CBF terminal projection fields. ChAT assays from 192 IgG-saporin-treated animals showed significant time-dependent decreases in ChAT activity in the neocortex, olfactory bulb and hippocampus, compared to PBS- or OKT1-saporin-injected controls. ChAT and tyrosine hydroxylase activity in the striatum was always unchanged by 192 IgG-saporin. ChAT immunohistochemistry was confirmative of major cell loss in the CBF, while other cholinergic nuclei appeared unremarkable. The data provide further evidence of the selectivity of 192 IgG-saporin in abolishing cholinergic, NGF receptor-positive CNS neurons.

Immunohistochemical detection of a monoclonal antibody directed against the NGF receptor in basal forebrain neurons following intraventricular injection.

It has been shown by autoradiography that, following intraventricular administration, a monoclonal antibody directed against the rat nerve growth factor (NGF) receptor is specifically accumulated bilaterally by numerous cholinergic neurons of the basal forebrain. This is consistent with the evidence that cholinergic basal forebrain neurons have NGF receptors and respond to NGF under a variety of experimental conditions. The present study demonstrates that the immunohistochemical detection of unmodified monoclonal antibody in cholinergic forebrain neurons following transport from CSF is feasible, although injection of larger amounts of the antibody is required to obtain an image equivalent to the one obtained with the autoradiographic method. The location of the immunohistochemical product clearly indicates that the antibody has been internalized, probably in an endosomal compartment.