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Copyright of Rechtsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Mathematic abilities in childhood are highly predictive for long-term neurocognitive outcomes. Preterm-born individuals have an increased risk for both persistent cognitive impairments and long-term changes in macroscopic brain organization. We hypothesized that the association of childhood mathematic abilities with both adulthood general cognitive abilities and associated fronto-parietal intrinsic networks is altered after preterm delivery. 72 preterm- and 71 term-born individuals underwent standardized mathematic and IQ testing at 8 years and resting-state fMRI and full-scale IQ testing at 26 years of age. Outcome measure for intrinsic networks was intrinsic functional connectivity (iFC). Controlling for IQ at age eight, mathematic abilities in childhood were significantly stronger positively associated with adults' IQ in preterm compared with term-born individuals. In preterm-born individuals, the association of children's mathematic abilities and adults' fronto-parietal iFC was altered. Likewise, fronto-parietal iFC was distinctively linked with preterm- and term-born adults' IQ. Results provide evidence that preterm birth alters the link of mathematic abilities in childhood and general cognitive abilities and fronto-parietal intrinsic networks in adulthood. Data suggest a distinct functional role of intrinsic fronto-parietal networks for preterm individuals with respect to mathematic abilities and that these networks together with associated children's mathematic abilities may represent potential neurocognitive targets for early intervention. [ABSTRACT FROM AUTHOR]

Preterm birth is a leading cause for impaired neurocognitive development with an increased risk for persistent cognitive deficits in adulthood. In newborns, preterm birth is associated with interrelated white matter (WM) alterations and deep gray matter (GM) loss; however, little is known about the persistence and relevance of these subcortical brain changes. We tested the hypothesis that the pattern of correspondent subcortical WM and GM changes is present in preterm-born adults and has a brain-injury-like nature, i.e., it predicts lowered general cognitive performance. Eighty-five preterm-born and 69 matched term-born adults were assessed by diffusion- and T1-weighted MRI and cognitive testing. Main outcome measures were fractional anisotropy of water diffusion for WM property, GM volume for GM property, and full-scale IQ for cognitive performance. In preterm-born adults, reduced fractional anisotropy was widely distributed ranging from cerebellum to brainstem to hemispheres. GM volume was reduced in the thalamus, striatum, temporal cortices, and increased in the cingulate cortices. Fractional anisotropy reductions were specifically associated with GM loss in thalamus and striatum, with correlation patterns for both regions extensively overlapping in the WM of brainstem and hemispheres. For overlap regions, fractional anisotropy was positively related with both gestational age and full-scale IQ. Results provide evidence for extensive, interrelated, and adverse WM and GM subcortical changes in preterm-born adults. Data suggest persistent brain-injury-like changes of subcortical-cortical connectivity after preterm delivery. [ABSTRACT FROM AUTHOR]

Copyright of Rechtsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Based on a recent finding that an Azospirillum isolate ASP-1 possessing high 16S rDNA similarity to Azospirillum irakense was able to degrade desferrioxamine type siderophores (Winkelmann et al. BioMetals 9, 78-83, 1996), various members of the genus Azospirillum were analyzed for their ability to degrade desferrioxamines. While the desferrioxamine-degrading activity was absent or scarcely detectable in strains of A. lipoferum, A. brasilense, A. amazonense, degradation activity seemed to be confined to the species A. irakense (KBC-1, KA3). Also the identity of strain ASP-1 as A. irakense could be confirmed by species-specific oligonucleotide hybridization, InterLINE PCR fingerprinting and carbon source utilization pattern (BIOLOG) analysis. Products of desferrioxamine B degradation were analyzed by analytical HPLC and HPLC/electrospray mass spectrometry. Using whole cells and purified enzyme it was shown that the trihydroxamate desferrioxamine B (561 amu) is split at the N-terminal amide bond yielding a monohydroxamate (MH1, 219 amu) and a dihydroxamate (DH1, 361 amu) metabolite. A second monohydroxamate (MH2, 319 amu) resulted from DH1 after splitting the acetylhydroxamate bond. Minor amounts of a further dihydroxamate (DH2, 419 amu) originated from splitting the second amide bond in desferrioxamine B. In addition to desferrioxamine B, several other linear and cyclic desferrioxamines and derivatives were degraded, whereas desferricoprogen and desferri-ferrichrome were not degraded, indicating high substrate specificity of the desferrioxamine hydrolase in A. irakense species. A simple microtiter plate assay was developed which can be used to phenotypically discriminate and identify species of A. irakense from other Azospirillum species by their characteristic feature of desferrioxamine degradation. [ABSTRACT FROM AUTHOR]

Optical gain on the 476.5 nm Ar II 4 p−4 s ion laser transition has been observed in argon-gas excited by 2.5 ns pulses of 90 MeVS ions with a repetition rate of 4883 Hz. The energy per pulse was 23 μJ. The projectiles were stopped in the target at pressures between 5 and 20 kPa. Gain was determined from a measured transient increase of the intensity of a 476.5 nm probe laser beam sent along the ion beam axis and back reflected by an aluminum foil. The maximum gain observed was (0.4±0.1)×10 at a target-gas pressure of 5 kPa. Control experiments using krypton as target-gas were performed and yielded a null result. The optical gain observed in argon is consistent with the result from an analysis of spectroscopic studies of rare-gas targets excited by heavy ion beams. [ABSTRACT FROM AUTHOR]

This article reviews the current criteria for diagnosis of Attention-Deficit Hyperactivity Disorder and Undifferentiated Attention-Deficit Disorder, according to the American Psychiatric Association, and describes other typical presenting features of children with attentional disorders. The current theories of the biological basis of attentional disorders are reviewed. Treatments of attentional disorders are discussed, including medical treatments with stimulants and tricyclic antidepressants, and non-medical treatments, such as behavior modification, psychotherapy, diets, and specific educational modifications that are felt to be helpful. Finally, our current thinking about the long-term outlook for children with attentional disorders is summarized. [ABSTRACT FROM AUTHOR]

Copyright of Archiv für Gynäkologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In nine patients with hemolytic-uremic syndrome, the plasma activity and plasma concentrations of antithrombin III were determined on admission to the hospital and during the clinical course of the disease. Hemodialysis was necessary in six of the patients. In seven children the plasma AT III activity was moderately to markedly below the lower limit of normal at 75%, and did not rise after plasmapheresis with fresh frozen plasma. Replacement therapy with AT III concentrate was started in these patients. During the first 2 days an average dose of AT III concentrate of 2.1 U/kg in 24 h was necessary to raise plasma AT III activity by 1%. No side effects were observed. An already pre-existing procoagulant status and the administration of heparin may lead to AT III deficiency in hemolytic-uremic syndrome. [ABSTRACT FROM AUTHOR]

Copyright of Archiv für Klinische und Experimentelle Dermatologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The emission of light from rare gas targets at pressures of more than 100 Pa excited by a pulsed heavy ion beam has been studied. The absolute intensity of several spectral lines has been measured as a function of time at different target gas pressures. Population densities, excitation cross sections, and rate constants for collisional quenching were determined from the line intensities and the lifetimes of the excited states. [ABSTRACT FROM AUTHOR]