Aufnahme von Trypanblau und Ferritin in die Blasenzellen des Bindegewebes von Helix pomatia und Cepaea nemoralis (Stylommatophora,Pulmonata)

Zusammenfassung Untersuchungen des Bindegewebes der stylommatophoren Pulmonaten Helix pomatia and Cepaea nemoralis zeigen, daß die Blasenzellen des Bindegewebes befähigt sind, Substanzen aus der Hämolymphe aufzunehmen. Licht- und elektronenmikroskopische Untersuchungen ausgewählter Bindegewebsbereiche, die in bestimmten Zeitintervallen nach der Injektion von Trypanblau oder Ferritin in die Körperhöhle präpariert wurden (Stufenuntersuchungen), ergaben, daß — mit Ausnahme einiger Blutzellen — ausschließlich die Blasenzellen die injizierten Substanzen aufgenommen hatten. Weder andere Bindegewebszellen noch die Zellen von Organen (u.a. Gonaden, Schlundringganglien), die von Bindegewebe umgeben werden, enthielten diese Substanzen oder hatten sie akkumuliert. Die elektronenmikroskopischen Aufnahmen zeigen, daß die Aufnahme von Ferritin in die Blasenzellen wahrscheinlich durch Pinocytose erfolgt.

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Uptake of trypan blue and ferritin into the globular cells of the connective tissue of Helix pomatia and Cepaea nemoralis (Stylommatophora, Pulmonata)

Summary Investigations of the connective tissue of the stylommatophoran pulmonates Helix pomatia and Cepaea nemoralis have demonstrated, that so-called globular cells have the capability for the uptake of substances out of the hemolymph. Light- and electron-microscopic investigations of pieces of connective tissues fixed at different intervals after the injection of Trypane Blue or Ferritin into the cavity of the body give striking evidence for the uptake of these substances exclusively into the globular cells (with the exception of some blood cells). Neither other connective tissue cells nor cells of the organs (e.g. gonads, central nervous ganglions) surrounded by connective tissue incorporate or accumulate the injected substances. The uptake of Ferritin into the cytoplasm of the globular cells, normally filled with a high amount of glycogen, takes place by pinocytosis.

     

Lipid composition and trophic relationships of krill species in a high Arctic fjord

Our study deals with the lipid biochemistry of the krill community in the ecosystem of the high Arctic Kongsfjord (Svalbard). During the last decades, Kongsfjord experienced a change in krill species composition due to recent increased advection of Atlantic water masses carrying characteristic boreal as well as subtropical-boreal euphausiids into the ecosystem. The lipid biochemistry and trophic relationships of the species recently inhabiting the Arctic water masses are scarcely known, although a change in a krill population may have a significant impact on the ecosystem. A comparison of nutrition and energy storage strategies, stable isotopes, lipid profiles and fatty acid compositions showed remarkable differences between the krill species. These reflected the diverse feeding behaviours and specific adaptations to the environments of their origin: the boreal Meganyctiphanes norvegica and subtropical Nematoscelis megalops appear more carnivorous and have significantly lower mean lipid contents (29 and 10 %, respectively) and a different energy storage pattern (triacylglycerols and polar lipids, respectively) than the arcto-boreal Thysanoessa inermis, which consists of up to 54 % of lipids mainly stored as wax esters (>40 %). These differences may have significant implications for the rapidly changing marine food web of Kongsfjord—especially for higher trophic levels relying on the nutritional input of animal lipids.     

Encapsulation of rat hepatocyte spheroids for the development of artificial liver

Hepatocyte spheroids and hepatocyte were immobilized in chitosan/alginate capsules formed by the electrostatic interactions between chitosan and alginate. After encapsulation, there was a 10% decrease in the viability of spheroids due to the exposure of the cells to a pH 6 during the encapsulation process. However, the encapsulated hepatocyte spheroids maintained over 50% viability and liver specific functions for 2 weeks while the encapsulated hepatocytes, free hepatocytes and free hepatocyte spheroids showed low viability and liver specific functions. Therefore, encapsulated hepatocyte spheroid might be applied to the development of a bioartificial liver.     

Algorithm of OMA for large-scale orthology inference

Background  

OMA is a project that aims to identify orthologs within publicly available, complete genomes. With 657 genomes analyzed to date, OMA is one of the largest projects of its kind.     

Chronic hypoxia alters the function of NOS nerves in cerebral arteries of near-term fetal and adult sheep.

In addition to adrenergic innervation, cerebral arteries also contain neuronal nitric oxide synthase (nNOS)-expressing nerves that augment adrenergic nerve function. We examined the impact of development and chronic high-altitude hypoxia (3,820 m) on nNOS nerve function in near-term fetal and adult sheep middle cerebral arteries (MCA). Electrical stimulation-evoked release of norepinephrine (NE) was measured with HPLC and electrochemical detection, whereas nitric oxide (NO) release was measured by chemiluminescence. An inhibitor of NO synthase, N(omega)-nitro-l-arginine methyl ester (l-NAME), significantly inhibited stimulation-evoked NE release in MCA from normoxic fetal and adult sheep with no effect in MCA from hypoxic animals. Addition of the NO donor S-nitroso-N-acetyl-dl-penicillamine fully reversed the effect of l-NAME in MCA from normoxic animals with no effect in MCA from hypoxic animals. Electrical stimulation caused a significant increase in NO release in MCA from normoxic animals, an effect that was blocked by the neurotoxin tetrodotoxin, whereas there was no increase in NO release in MCA from hypoxic animals. Relative abundance of nNOS as measured by Western blot analysis was similar in normoxic fetal and adult MCA. However, after hypoxic acclimitization, nNOS levels dramatically declined in both fetal and adult MCA. These data suggest that the function of nNOS nerves declines during chronic high-altitude hypoxia, a functional change that may be related to a decline in nNOS protein levels.     

DEAR1 Is a Dominant Regulator of Acinar Morphogenesis and an Independent Predictor of Local Recurrence-Free Survival in Early-Onset Breast Cancer

Background

Breast cancer in young women tends to have a natural history of aggressive disease for which rates of recurrence are higher than in breast cancers detected later in life. Little is known about the genetic pathways that underlie early-onset breast cancer. Here we report the discovery of DEAR1 (ductal epithelium–associated RING Chromosome 1), a novel gene encoding a member of the TRIM (tripartite motif) subfamily of RING finger proteins, and provide evidence for its role as a dominant regulator of acinar morphogenesis in the mammary gland and as an independent predictor of local recurrence-free survival in early-onset breast cancer.

Methods and Findings

Suppression subtractive hybridization identified DEAR1 as a novel gene mapping to a region of high-frequency loss of heterozygosity (LOH) in a number of histologically diverse human cancers within Chromosome 1p35.1. In the breast epithelium, DEAR1 expression is limited to the ductal and glandular epithelium and is down-regulated in transition to ductal carcinoma in situ (DCIS), an early histologic stage in breast tumorigenesis. DEAR1 missense mutations and homozygous deletion (HD) were discovered in breast cancer cell lines and tumor samples. Introduction of the DEAR1 wild type and not the missense mutant alleles to complement a mutation in a breast cancer cell line, derived from a 36-year-old female with invasive breast cancer, initiated acinar morphogenesis in three-dimensional (3D) basement membrane culture and restored tissue architecture reminiscent of normal acinar structures in the mammary gland in vivo. Stable knockdown of DEAR1 in immortalized human mammary epithelial cells (HMECs) recapitulated the growth in 3D culture of breast cancer cell lines containing mutated DEAR1, in that shDEAR1 clones demonstrated disruption of tissue architecture, loss of apical basal polarity, diffuse apoptosis, and failure of lumen formation. Furthermore, immunohistochemical staining of a tissue microarray from a cohort of 123 young female breast cancer patients with a 20-year follow-up indicated that in early-onset breast cancer, DEAR1 expression serves as an independent predictor of local recurrence-free survival and correlates significantly with strong family history of breast cancer and the triple-negative phenotype (ER⁻, PR⁻, HER-2⁻) of breast cancers with poor prognosis.

Conclusions

Our data provide compelling evidence for the genetic alteration and loss of expression of DEAR1 in breast cancer, for the functional role of DEAR1 in the dominant regulation of acinar morphogenesis in 3D culture, and for the potential utility of an immunohistochemical assay for DEAR1 expression as an independent prognostic marker for stratification of early-onset disease.     

A domesticated transposon mediates the effects of a single‐nucleotide polymorphism responsible for enhanced muscle growth

Single‐nucleotide polymorphisms (SNPs) in the regulatory regions of the genome can have a profound impact on phenotype. The G3072A polymorphism in intron 3 of insulin‐like growth factor 2 (IGF2) is implicated in higher muscle content and reduced fat in European pigs and is bound by a putative repressor. Here, we identify this repressor—which we call muscle growth regulator (MGR)—by using a DNA protein interaction screen based on quantitative mass spectrometry. MGR has a bipartite nuclear localization signal, two BED‐type zinc fingers and is highly conserved between placental mammals. Surprisingly, the gene is located in an intron and belongs to the hobo‐Ac‐Tam3 transposase superfamily, suggesting regulatory use of a formerly parasitic element. In transactivation assays, MGR differentially represses the expression of the two SNP variants. Knockdown of MGR in C2C12 myoblast cells upregulates Igf2 expression and mild overexpression retards growth. Thus, MGR is the repressor responsible for enhanced muscle growth in the IGF2 G3072A polymorphism in commercially bred pigs.