Die Rassenfrage bei Culex pipiens in Deutschland

Zusammenfassung Auch für Deutschland müssen wenigstens 2 verschiedene Rassen vonCulex pipiens als bewiesen gelten, die mit den vonRoubaud aufgestellten RassenC. p. pipiens undC. p. autogenicus identisch sein dürften. Die letztere Rasse, die in Hamburg unter anderem in einem Kinderkrankenhaus gefunden wurde, ist vor allem dadurch gekennzeichnet, da\ sie zur Entwicklung der Eier keine Blutnahrung benötigt, sondern allein auf Grund der im Larvalleben gespeicherten Reservestoffe reife Eier zu bilden vermag. Diese Eigenschaft ist auch an dem Entwicklungszustand des Ovars erkennbar. Da bei der autogenen Rasse das Ovar nach dem Schlüpfen und vor der Eiablage fast stets wesentlich weiter als bei der nichtautogenen Rasse vor der Blutaufnahme entwickelt ist, lassen sich die beiden Rassen hierdurch leicht unterscheiden. Dieses Merkmal hat für die Diagnose der Rassen und der autogenen Eigenschaft bei Mischpopulationen deshalb besondere Bedeutung, weil in autogenen StÄmmen (wenigstens im Laboratorium) nur ein Teil der Vollreife Eier bildet, bei den übrigen aber die Entwicklung des Ovars stehen bleibt, sofern der Mücke nicht Gelegenheit zum Blutsaugen geboten wird. ZÄhlt man in einer Zucht oder Population nur die autogenen Gelege, so erfa\t man damit nur einen Teil der wirklich autogenen . Die Unterschiede im Entwicklungszustand des Ovars reichen bis in das letzte Larvenstadium zurück. Die beiden Rassen verhalten sich auch sonst physiologisch (Begattungs- und überwinterungsgewohnheiten, Form und Grö\e der Gelege usw.), wie die vonRoubaud beschriebenen. Im Anschlu\ wird ein erfolgreiches Kreuzungsexperiment zwischen der autogenen und der typischen Rasse beschrieben und die Vererbung der autogenen Eigenschaft in den nÄchstfolgenden Generationen analysiert.     

Solution behaviour of a liquid-crystalline side-group polymer

Dilute and semidilute solutions of fractions of a liquid-crystalline side-group polymer were investigated by means of size-exclusion chromatography (SEC), static light scattering (LS), density and viscosity measurements. The mass-average molar mass ranged from M?_w = 1 · 10⁵ g · mol^?1 to 1,5 · 10⁶ g · mol^?1. Large discrepancies were found between the molar mass determined through SEC and through LS. Strong interactions between the mesogenic groups can be assumed by the results of density and LS measurements. Due to the determined characteristic ratio of C_∞ = 19,5 a similar chain stiffness as a poly(alkyl methacrylate) of equal length of the side chain is observed. In semidilute solutions an excess low-angle scattering (ExLAS) occurs which increases at higher concentrations. The dependence of the reduced osmotic modulus [M?_w/(RT)](?π/?c)_T on the parameter x = A₂ · M?_W · c was studied.     

Lymphoma-like presentation of acute monocytic leukaemia

Four patients in whom a diagnosis of acute monocytic leukaemia (M5) was subsequently made presented with extramedullary disease clinically resembling lymphoma. In all patients histological sections were initially misinterpreted as showing malignant lymphoma or anaplastic carcinoma. The diagnosis of M5 leukaemia was subsequently made on the basis of morphological and cytochemical studies of peripheral blood and bone marrow. The histological diagnosis of the soft tissue lesions of M5 leukaemia (monocytic sarcoma) is difficult, although features such as abundant cytoplasm and the presence of some reniform nuclei are helpful. If there is no peripheral blood or bone marrow involvement and only fixed paraffin-embedded tissues are available, demonstration of lysozyme by an immunoperoxidase technique may confirm the diagnosis but results are not invariably positive. An early diagnosis of M5 leukaemia has therapeutic implications since the disease evolves through a progressive leukaemia phase and systemic therapy is essential.     

Immature B cells from human and mouse bone marrow can change their surface light chain expression

The capacity of bone marrow-derived surface immunoglobulin-positive (sIg⁺) human and mouse immature B cells, generated either in vitro or in vivo, to change their light (L) chain expression, has been assayed by the number of cells which change in vitro from one type of L chain to the other type, or to no sIg at all. Immature sIg⁺ B cells were generated in vitro from sIg^? precursor cells from human or mouse bone marrow. The immature sIg⁺ cells expressed RAG-1. Human sIg⁺ cells expressed xfr; and λ L chains in ratios between 1:1 and 3:1, whereas in mouse cells, this ratio ranged from 10:1 to 20:1. Upon reculture of the human and mouse xfr;⁺sIg⁺ cells, about half of them remained xfr;⁺, a quarter became λ⁺, and another quarter became sIg^?. Between 1 and 3% expressed both xfr; and λ chains. Of the human λ⁺ cells, about two-thirds remained λ⁺, only 1 to 2% became xfr;⁺, while the other third became sIg^?. Again, between 1 and 3% expressed both xfr; and λ L chains. These results indicate that expression of sIgM in the B cell membrane does not terminate L chain gene rearrangement, and that some order exists in xfr; versus λ gene rearrangements. Hence, human and mouse xfr;⁺ immature B cells can become λ⁺, but very few of the λ⁺ cells can become xfr;⁺, and both can become sIg^?. Further, human CD10⁺/sIg⁺ xfr;⁺ and λ⁺ cells and mouse B220^low/sIg^low xfr;⁺ cells enriched from bone marrow, i.e. immature B cells differentiated in vivo, changed their Ig phenotype upon in vitro culture, but in lower frequencies. By contrast, human and mouse mature B cells did not change their L chain or Ig phenotype. Hence, at least a part of the sIg⁺ immature B cells in bone marrow retain the capacity to change their L chain and Ig phenotype, and this capacity is lost when they become mature, peripheral B cells.     

Cytologische Kriterien der Wirkung von Sanamycin

Zusammenfassung Die cytostatische Wirkung des Sanamycin auf Milz, Thymus und Nebennieren des Kaninchens wurde mit Hilfe einer vergleichenden cyto-histologischen Untersuchungtechnik geprüft, um einen näheren Einblick in die zellspezifischen Angriffspunkte des Medikamentes zu gewinnen. Der Effekt auf die normale Lymphopoese besteht in einer zeitlich begrenzten Abnahme der reifen Lymphocyten zugunsten einer Vermehrung der Lymphoblasten, wobei histologisch eine allgemeine Reduktion der lymphatischen Gewebsanteile in Erscheinung tritt. Das RHS bleibt in diesem Zusammenhang unberührt. Die Nebennieren zeigen nach hohen Sanamycindosen Veränderungen, die einer beträchtlichen Stresswirkung oder einer reversiblen toxischen Schäidgung entsprechen können. Das durch kurzfristige Sensibilisierung stimulierte Zellsubstrat der Antikörperbildung erfährt durch Sanamycingaben eine nachhaltige Depression, während dieser Effekt bei chronisch sensibilisierten Tieren wesentlich geringer ausgeprägt ist. Die tierexperimentell erhobenen Befunde werden im Hinblick auf die therapeutische Sanamycinwirkung bei lymphatischen Systemkrankheiten und die Möglichkeiteiner Beeinflussungakuter Antigen-Antikörperreaktionen diskutiert.Herrn Professor Dr.R. Schoen zum 65. Geburtstag.     

Complex mosaic structural variations in human fetal brains

Somatic mosaicism, manifesting as single nucleotide variants (SNVs), mobile element insertions, and structural changes in the DNA, is a common phenomenon in human brain cells, with potential functional consequences. Using a clonal approach, we previously detected 200–400 mosaic SNVs per cell in three human fetal brains (15–21 wk postconception). However, structural variation in the human fetal brain has not yet been investigated. Here, we discover and validate four mosaic structural variants (SVs) in the same brains and resolve their precise breakpoints. The SVs were of kilobase scale and complex, consisting of deletion(s) and rearranged genomic fragments, which sometimes originated from different chromosomes. Sequences at the breakpoints of these rearrangements had microhomologies, suggesting their origin from replication errors. One SV was found in two clones, and we timed its origin to ∼14 wk postconception. No large scale mosaic copy number variants (CNVs) were detectable in normal fetal human brains, suggesting that previously reported megabase-scale CNVs in neurons arise at later stages of development. By reanalysis of public single nuclei data from adult brain neurons, we detected an extrachromosomal circular DNA event. Our study reveals the existence of mosaic SVs in the developing human brain, likely arising from cell proliferation during mid-neurogenesis. Although relatively rare compared to SNVs and present in ∼10% of neurons, SVs in developing human brain affect a comparable number of bases in the genome (∼6200 vs. ∼4000 bp), implying that they may have similar functional consequences.

Somatic mosaicism, the presence of more than one genotype in the somatic cells of an individual, is a prominent phenomenon in the human central nervous system. Forms of mosaicism include aneuploidies and smaller copy number variants (CNVs), structural variants (SVs), mobile element insertions, indels, and single nucleotide variants (SNVs). The developing human brain exhibits high levels of aneuploidy compared to other tissues, generating genetic diversity in neurons (Pack et al. 2005; Yurov et al. 2007; Bushman and Chun 2013). Such aneuploidy was suggested to be a natural feature of neurons, rather than a distinctive feature of neurodegeneration. However, the frequency of aneuploidy in neurons has been debated, with a separate study suggesting that aneuploidies occur in only about 2.2% of mature adult neurons (Knouse et al. 2014). They hence infer that such aneuploidy could have adverse effects at the cellular and organismal levels. Additionally, analysis of single cells from normal and pathological human brains identified large, private, and likely clonal somatic CNVs in both normal and diseased brains (Gole et al. 2013; McConnell et al. 2013; Cai et al. 2014; Knouse et al. 2016; Chronister et al. 2019; Perez-Rodriguez et al. 2019), with 3%–25% of human cerebral cortical nuclei carrying megabase-scale CNVs (Chronister et al. 2019) and deletions being twice as common as duplications (McConnell et al. 2013). Given that CNVs often arise from nonhomologous recombination and replication errors, their likely time of origin is during brain development. However, when CNVs first arise in human brain development has not yet been investigated. The present work is the first to examine this question using clonal populations of neuronal progenitor cells (NPCs) obtained from fetal human brains.Detection of CNVs in single neurons is challenging, given the need to amplify DNA. Such amplification may introduce artifacts that could, in turn, be misinterpreted as CNVs. In order to address this technical limitation, Hazen et al. reprogrammed adult postmitotic neurons using somatic cell nuclear transfer (SCNT) of neuronal nuclei into enucleated oocytes (Hazen et al. 2016). These oocytes then made sufficient copies of the neuronal genome allowing for whole-genome sequencing (WGS), thus eliminating the need for amplification in vitro. Using this method, they identified a total of nine structural variants in six neurons from mice, three of which were complex rearrangements. However, it is not possible to extend such studies to humans, given the ethical issues involved, besides the technical challenges in obtaining and cloning adult neurons. To circumvent the need of single-cell DNA amplification or nuclear cloning, we examined clonal cell populations obtained from neural progenitor cells from the frontal region of the cerebral cortex (FR), parietal cortex (PA) and basal ganglia (BG) and describe here the discovery and analysis of mosaic SVs in these NPCs (Bae et al. 2018). These clones were sequenced at 30× coverage (much higher than most previous single-cell studies), allowing identification of SVs other than large deletions and duplications as well as precise breakpoint resolution.     

Characterization of a Helicobacter pylori neutrophil-activating protein.

Helicobacter pylori-associated gastritis is mainly an inflammatory cell response. In earlier work we showed that activation of human neutrophils by a cell-free water extract of H. pylori is characterized by increased expression of neutrophil CD11b/CD18 and increased adhesiveness to endothelial cells. The work reported here indicates that the neutrophil-activating factor is a 150,000-molecular-weight protein (150K protein). Neutrophil proadhesive activity copurified with this protein, which is a polymer of identical 15K subunits. Specific antibody, prepared against the purified 15K subunit, neutralized the proadhesive activity of the pure protein and of water extracts obtained from different strains of H. pylori. The gene (napA) for this protein (termed HP-NAP, for H. pylori neutrophil-activating protein) was detected, by PCR amplification, in all of the H. pylori isolates tested; however, there was considerable strain variation in the level of expression of HP-NAP activity in vitro. HP-NAP could play an important role in the gastric inflammatory response to H. pylori infection.     

Virus persists in beta cells of islets of Langerhans and infection is associated with chemical manifestations of diabetes. II. Morphologic observations.

Persistence of lymphocytic choriomeningitis (LCM) virus in the islets of Langerhans was associated with mild hyperglycemia and abnormal glucose tolerance test results. Early histopathologic events consisted of occasional perivascular inflammatory mononuclear cells around both islet and acinar cells. Morphometric studies showed an increase in the size of islets from virus-infected mice. By electron microscopy, LCM virions were found within infected beta cells. Cytolytic injury of beta cells was minimal and did not account for the abnormalities of glucose metabolism. In contrast to the findings in islets, ultrastructural studies of acinar cells revealed LCM virions in abundance, vacuolar degeneration, and intracytoplasmic inclusions. This study extends the previous observation that LCM virus infection may persist in beta cells of the islets of Langerhans without causing structural injury but be associated with abnormalities resembling the chemical and histopathologic features of the early stage of Type II (adult-onset) human diabetes mellitus.