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Measurements of radiative branching ratios of K x-ray transitions in Cr21+, Mn22+, Fe23+, Ni25+, and Ge29+
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Precision measurement of the K alpha transitions in heliumlike Ge30+
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Measurement of level-specific dielectronic-recombination cross sections of heliumlike Fe XXV.
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Measurements of line overlap for resonant photopumping of 4-->4 transitions in highly charged nickel-like ions.
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Experimental strategies for modification of histocompatibility antigens in tumor cells.
Cancer may be thought of as an immunological disorder that arises because certain 'transformed' cells, endowed with the propensity to divide, have learned to evade detection by the immune system. The prospect of intervention by 'immunotherapy' depends very much on our ability to either [1] render cancer cells more recognizable to the immune system, or [2] potentiate the immune system towards a more effective recognition of cancer cells. There is now direct evidence that suppression of the major histocompatibility complex class I antigens, a family of cell-surface glycoproteins required for the presentation of cancer cells to the immune system, is directly responsible for the ability of tumor cells to escape immune surveillance. It has been shown that cancer cells can be made immunogenic either by the expression of an exogenous class I gene introduced by DNA-mediated gene transfer, or by the derepression of endogenous class I genes with interferon; these cells are efficiently rejected by the immune system. Even more interesting is the finding that the immune system can be potentiated to reject tumors by immunization with homologous tumor cells that have been manipulated to express normal levels of class I antigens. Since increasing numbers of human tumors have been found to have greatly reduced levels of class I antigens, these findings suggest a direct route to immunotherapy that involves debulking of the tumor mass, raising the level of class I antigens in a small number of explanted tumor cells, and re-immunizing the host.
An evaluation of the course of peripheral neuropathies based on clinical and neurographical re-examinations.
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Use of phylogeny to resolve the taxonomy of the widespread and highly polymorphic African giant shrews (Crocidura olivieri group, Crocidurinae, Mammalia).
The aim of this study is to provide a better understanding of the genetic relationships within the widespread and highly polymorphic group of African giant shrews (Crocidura olivieri group). We sequenced 769 base pairs (bp) of the mitochondrial cytochrome b gene and 472 bp of the mitochondrial control region over the entire geographic range from South Africa to Morocco. The analyses reveal four main clades associated with different biomes. The largest clade occurs over a range covering Northwest and Central Africa and includes samples of C. fulvastra, C. olivieri, and C. viaria. The second clade is composed of C. goliath from Gabon, while South African C. flavescens, and C. hirta form two additional clades. On the basis of these results, the validity of some taxa in the C. olivieri group should be re-evaluated.
Electron-impact ionization of lithiumlike ions: Ti19+, V20+, Cr21+, Mn22+, and Fe23+
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Indirect x-ray line formation processes in highly charged barium.
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Georg Schmorl on trophoblasts in the maternal circulation.
Trafficking of cells between the fetus and its mother provides indirect clues to the underlying pathophysiology of pregnancy. Georg Schmorl first documented the presence of fetal cells in the maternal body and emphasized the importance of the placenta in eclampsia. Although his classic paper, written in 1893, is widely cited today, few investigators have actually read the paper, as it was published in German [Schmorl G., Pathologisch-anatomische Untersuchungen über Puerperal-Eklampsie. Verlag FCW Vogel, Leipzig; 1893]. Our goal was to translate the paper into English and critically re-evaluate its conclusions from a 21st century perspective. Schmorl was remarkably astute in his assessment of the pathologic changes that were seen in the 17 women on whom he performed complete autopsies. He found similar severe changes in all of the women, implying a common pathogenesis. This was in direct contrast to the then current doctrine. He was the first to observe the presence of thrombi containing multinucleated syncytial giant cells in the lungs of the women and speculated that they were of placental origin. To support his hypothesis he performed animal experiments. He also recognized that feto-maternal trafficking occurred in normal gestations but was increased in pregnancies affected by eclampsia. Using sophisticated molecular techniques we can now precisely confirm what Schmorl so elegantly described.
Antithrombotic properties of a direct thrombin inhibitor with a prolonged half-life and AT-mediated factor Xa inhibitory activity.
Rebound thrombin generation after successful thrombolysis might be related to (i) too short-term anticoagulant therapy and to (ii) the inability of heparin derivatives to inhibit clot-bound thrombin. To meet these shortcomings, a compound was synthesized, which consists of a pentasaccharide conjugated to a direct thrombin inhibitor. This compound (Org 42675) has a 10 times longer half-life compared with the original half-life of the direct thrombin inhibitor, while the thrombin inhibitory activity is maintained. An extra advantage of this product is the inhibitory activity on thrombin generation via antithrombin III (AT)-mediated factor (F)Xa inhibition. Org 42675 inhibited in vitro clot-bound thrombin with similar activity to the direct thrombin inhibitor argatroban. In experimental models in rats, Org 42675 showed on a molar base similar antithrombotic activity to unfractionated heparin, was more active than argatroban and was more active than fondaparinux sodium (AT-mediated FXa inhibitor) in arterial thrombosis. Finally, Org 42675 was far more active than the three reference compounds in an experimental thrombolysis model in rabbits. These properties of Org 42675, with its FXa and (clot-bound) thrombin inhibitory activity in combination with its long half-life, make this compound a powerful drug that is likely to be effective in the prevention of re-occlusion after successful thrombolysis in man.
The neurological mutant quaking(viable) is Parkin deficient.
The mouse mutant quaking(viable) ( qk(v)) has been studied for almost four decades as a model for dysmyelination of the central nervous system (CNS). The genetic lesion associated with the qk(v) phenotype is a large deletion of approximately 1 Megabase on mouse Chromosome (Chr) 17. This deficiency alters the expression of transcripts from the qkI locus in oligodendrocytes, resulting in improper myelination of the CNS in animals homozygous for the deletion. To determine whether other genes within the deletion contribute to the quaking(viable) phenotype, we physically mapped and sequenced the deleted interval. We determined that the mouse Parkin gene, as well as the Parkin co-regulated gene ( Pacrg), lies within the qk(v) deletion. We determined that qk(v) mutants completely lack the expression of the Parkin gene product. Loss-of-function mutations in the human PARKIN gene cause autosomal juvenile Parkinson's disease (AR-JP). Our studies show that the deletion of Parkin in qk(v) brains does not result in the loss of dopaminergic neurons typical of AR-JP patients. Also, alpha-synuclein, a target of Parkin-dependent ubiquitination, does not accumulate in qk(v) mutant brains. Despite the lack of AR-JP-like neuropathology in qk(v) mice, this mutant may constitute a readily available model for the study of the cellular function of Parkin. This is the first report of a gene distinct from qkI affected by the qk(v) deletion. The discovery of the multigenic nature of this classical mouse mutation calls for the re-evaluation of its phenotypic characterization.
Pliocene and Pleistocene diversification and multiple refugia in a Eurasian shrew (Crocidura suaveolens group).
We sequenced 998 base pairs (bp) of mitochondrial DNA cytochrome b and 799 bp of nuclear gene BRCA1 in the Lesser white-toothed shrew (Crocidura suaveolens group) over its geographic range from Portugal to Japan. The aims of the study were to identify the main clades within the group and respective refugia resulting from Pleistocene glaciations. Analyses revealed the Asian lesser white-toothed shrew (C. shantungensis) as the basal clade, followed by a major branch of C. suaveolens, subdivided sensu stricto into six clades, which split-up in the Upper Pliocene and Lower Pleistocene (1.9-0.9 Myr). The largest clade, occurring over a huge range from east Europe to Mongolia, shows evidence of population expansion after a bottleneck. West European clades originated from Iberian and Italo-Balkanic refugia. In the Near East, three clades evolved in an apparent hotspot of refugia (west Turkey, south-west and south-east of the Caucasus). Most clades include specimens of different morphotypes and the validity of many taxa in the C. suaveolens group has to be re-evaluated.
Morphological analogies of fetal prostate stroma and stromal nodules in BPH.
BACKGROUND: A "reawakening" of ontogenetic processes in the development of BPH is still in debate. Therefore, morphological analogies of fetal prostate stroma and nodular stromal proliferates in BPH were investigated. METHODS: Fetal prostates (n = 30; weeks 12-40 of gestation) and stromal nodules of benign prostatic hyperplasia (n = 375 from autopsies, n = 100 from biopsies) were investigated by histo- and immunohistochemistry with special regard to cytoskeletal (alpha-actin, desmin, myosin, and vimentin), neuronal (S-100 protein), neuroendocrine (neuron-specific enolase), leukocytic (CD3, CD20, and CD68) and vascular (CD34, BMA-120, and factor VIII) antigens. RESULTS: The developing fetal prostate stroma consists of immature mesenchymal cells up to week 17 of gestation, followed by fibroblastic and fibromuscular stromal cells up to week 25 of gestation and predominantly smooth-muscular cells until the end of gestation. Stromal nodules occur as immature mesenchymal, fibroblastic, fibromuscular, and smooth-muscular, suggestive of a maturational process. The fetal prostate stroma and the stromal nodules present, with an increasing degree of maturation, a similar vascular pattern and a similar occurrence of CD3 (T-lymphocytes), CD20 (B-lymphocytes), CD68 (macrophages), S-100, and neuron-specific enolase-positive cells. CONCLUSIONS: The data suggest that ontogenetic processes are recapitulated in the development of stromal nodules in benign prostatic hyperplasia, supporting the idea of a "re-awakening" of fetal processes in BPH.
Re: Validation of the Gail et al. model for predicting individual breast cancer risk.
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[Femur head necrosis in the adult. Diagnosis, therapy, legal aspects for insurance medicine].
Early recognition and adequate therapy of necrosis of the head of the femur in adult patients in increasingly gaining importance since they considerably influence the permanent loss of function and reduction of the earning capacity of people of working age. Presently, MRT examination is the most conclusive method for the early stage of necrosis of the head of the femur. After the introduction of microsurgical methods, new therapeutic measures for avascular necrosis of the head of the femur are available, apart from conventional surgical methods to relieve the necrotic areas and the so-called metabolic irritation drilling. Direct vascular-supply, autologous, heterotopic, corticospongiose transplants in the necrotic head of the femur are suited to re-establish circulation in the necrotic area. This involves a considerable operative scope of work.
Re: tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study.
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