Einige Daten zum Blutbild des Rothirsches (Cervus elaphus L.)

Zusammenfassung Es werden einige Daten zur Kenntnis des Blutbildes vom Rothirsch (Cervus elaphus L.) mitgeteilt. In hämatologischer Beziehung besteht eine weitgehende Übereinstimmung mit den kleinen Wiederkäuern Schaf und Ziege, nach Leukozytenzahl und Saponinempfindlichkeit der Erythrozyten weist das Hirschblut deutliche Unterschiede gegenüber domestizierten Wiederkäuern auf.Unter Mitwirkung der med.-techn. Assistentin, Fräulein Sybille Buchheim.     

Anatomy of the Enigmatic Reptile Elachistosuchus huenei Janensch, 1949 (Reptilia: Diapsida) from the Upper Triassic of Germany and Its Relevance for the Origin of Sauria

The holotype and only known specimen of the enigmatic small reptile Elachistosuchus huenei Janensch, 1949 from the Upper Triassic (Norian) Arnstadt Formation of Saxony-Anhalt (Germany) is redescribed using μCT scans of the material. This re-examination revealed new information on the morphology of this taxon, including previously unknown parts of the skeleton such as the palate, braincase, and shoulder girdle. Elachistosuchus is diagnosed especially by the presence of the posterolateral process of the frontal, the extension of the maxillary tooth row to the posterior margin of the orbit, the free posterior process of the jugal, and the notched anterior margin of the interclavicle. Phylogenetic analyses using two recently published character-taxon matrices recovered conflicting results for the phylogenetic position of Elachistosuchus–either as an archosauromorph, as a lepidosauromorph or as a more basal, non-saurian diapsid. These different placements highlight the need of a thorough revision of critical taxa and new character sets used for inferring neodiapsid relationships.     

Histoplasmosis Outbreaks in Brazil: Lessons to Learn About Preventing Exposure

Mycopathologia - Histoplasmosis is considered the most common invasive opportunistic fungal disease in the Americas, with outbreaks and micro-epidemics reported for over 80 years. In...     

Modification of nonstructural protein 1 of influenza A virus by SUMO1

Nonstructural protein 1 (NS1) is one of the major factors resulting in the efficient infection rate and high level of virulence of influenza A virus. Although consisting of only approximately 230 amino acids, NS1 has the ability to interfere with several systems of the host viral defense. In the present study, we demonstrate that NS1 of the highly pathogenic avian influenza A/Duck/Hubei/L-1/2004 (H5N1) virus interacts with human Ubc9, which is the E2 conjugating enzyme for sumoylation, and we show that SUMO1 is conjugated to H5N1 NS1 in both transfected and infected cells. Furthermore, two lysine residues in the C terminus of NS1 were identified as SUMO1 acceptor sites. When the SUMO1 acceptor sites were removed by mutation, NS1 underwent rapid degradation. Studies of different influenza A virus strains of human and avian origin showed that the majority of viruses possess an NS1 protein that is modified by SUMO1, except for the recently emerged swine-origin influenza A virus (S-OIV) (H1N1). Interestingly, growth of a sumoylation-deficient WSN virus mutant was retarded compared to that of wild-type virus. Together, these results indicate that sumoylation enhances NS1 stability and thus promotes rapid growth of influenza A virus.     

Role of transmembrane GTPases in mitochondrial morphology and activity

Mitochondria play crucial role in the energetic metabolism, thermogenesis, maintenance of calcium homeostasis and apoptosis. Cyclic changes in fusion and fission of mitochondria are required for properly functioning organelles, especially in tissues with high dependence on energy supply such as skeletal muscles, heart, or neurons. The key role of mitochondrial fusion is observed in embryonic development and maintaining unchanged mtDNA pool under conditions of oxidative stress. There is a large number of data indicating that mitochondrial networks often accompany the resistance to apoptotic stimuli. In contrast to fusion--the mitochondrial fission precedes apoptosis. According to the newest knowledge precise interactions between a few proteins are required for mitochondrial fusion and division. Among them Drp1, Mfn1, Mfn2 and Opal are considered the most important. Recent reports shed some light on the physiological importance of proteins participating in mitochondrial membrane dynamics in energy production, apoptosis and cellular signaling. In this review the authors report on the recent knowledge concerning structural changes of mitochondria with a particular interest to transmembrane GTPases and their role in cellular physiology.     

New look at starch degradation in Arabidopsis thaliana L. chloroplasts

Transitory starch is accumulated during the day and is the main source of energy for the cell metabolism during the night. The observed periodical starch degradation has become a model often used by scientist in their experiments. Starch granule degradation could be divided into 2 periods: initiation of degradation and digestion of amylopectin and amylose into maltooligosaccharide and their derivative. Key meaning is attributed in this process to beta-amylaze, product of its activity beta-maltose is transported to the cytosole and there it subjects farthest conversions. It has been demonstrated that a number of enzymes take part in the starch degradation process. However, the way of regulating their activity is still not fully explained. There is most important elements effecting rate of starch decomposition: day cycle, starch phosphorylation and regulation of enzyme activity. It proceeds through redox potential, pH changes and phosphorylation of protein involved in starch degradation due specific phosphatases. The purpose of the current work is to systematize the knowledge of the Arabidopsis thaliana L. leaf starch degradation. The results of the recent research cast a new light on the starch degradation process as well as on its control.     

Mitofusin 2 (Mfn2): a key player in insulin-dependent myogenesis in vitro

We have previously shown that mitochondrial activity increases in response to insulin in differentiating muscle cells. Moreover, the protein kinase kinase/extracellular-signal-regulated kinase (MAPKK/ERK-MEK) inhibitor PD98059 accelerates insulin-mediated myogenesis, whereas the phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002 or blockade of mitochondrial respiration abrogates insulin-mediated myogenesis. Our present study focuses on the mitochondrial transmembrane protein, hyperplasia suppressor gene/mitofusin2 (HSG/Mfn2), which regulates both mitochondrial fusion (as demonstrated by perinuclear mitochondria clustering) and insulin-dependent myogenesis in vitro. Increased mitochondrial length and interconnectivity are not observed after the inhibition of PI3-K activity with LY294002. Insulin induces Mfn2 and subunits I and IV of cytochrome-c oxidase (MTCOI and NCOIV) in L6 myoblasts. Inhibition of the MEK-dependent signalling pathway elevates the Mfn-2 protein level. The molecular mechanism of this phenomenon is unknown, although immunoprecipitation studies indicate that, during insulin-mediated myogenesis, Ras protein (an upstream activator of the MAPK/ERK1/2 cascade) interacts with HSG/Mfn2 in muscle cells. Interaction of Ras with Mfn2 continues unless insulin is present and is reduced after PD98059 co-treatment indicating that insulin-mediated myogenesis is increased by the inhibition of MEK, most probably by the lack of mitogenic signals opposing muscle differentiation. We conclude that insulin-mediated myogenesis depends on PI3-K activity, which stimulates mitochondrial activity and the extensive fusion of mitochondria. We further suggest that insulin stimulates the expression of Mfn2 protein, which in turn binds to Ras and inhibits the MEK-dependent signalling pathway. At the same time, the PI3-K-dependent signalling pathway is boosted, mitochondrial respiration increases and the rate of myogenesis is accelerated. This work was supported by the State Committee for Scientific Research in Poland (grant no. 2 P06D 015 29) and by grant no. 117/E-385/SPB/COST/P-06/DWM within the framework of COST 925 Action on “The importance of prenatal events for postnatal muscle growth in relation to the quality of muscle based foods”.     

Localization of the iron-regulatory proteins hemojuvelin and transferrin receptor 2 to the basolateral membrane domain of hepatocytes

The newly discovered proteins hemojuvelin (Hjv) and transferrin receptor type 2 (TfR2) are involved in iron metabolism. Mutations in the Hjv and TfR2 gene cause hemochromatosis. We investigated the expression and cellular localization of Hjv and TfR2 in rat and human liver. The expression of Hjv and TfR2 was shown on mRNA and protein level by RT–PCR and immunoblot experiments. Their cellular localization was studied by immunofluorescence with antibodies raised against Hjv and TfR2. Hjv and TfR2 are present in human and rat liver and in primary human hepatocytes. Antisera raised against Hjv identified immunoreactive proteins with an apparent size of 44 and 46 kDa in immunoblot experiments of rat and human liver extracts, which are in accordance with the putative membrane-bound and cleaved soluble forms of this protein, respectively. TfR2 was detected as a 105 kDa protein corresponding to the predicted size of glycosylated TfR2 monomers. In immunofluorescence experiments, Hjv and TfR2 were found in rat liver only in hepatocytes. At the subcellular level, both proteins were predominantly localized to the basolateral membrane domain of hepatocytes. The localization of Hjv and TfR2 at the same membrane domain renders a functional interaction of these two proteins in iron homeostasis possible. Electronic Supplementary Material Supplementary material is available to authorised users in the online version of this article at . Kulaksiz and Stremmel contributed equally to this work.     

A three-dimensional model of CYP19 aromatase for structure-based drug design

Aromatase (CYP450_arom, CYP19) is an enzyme responsible for converting the aliphatic androgens androstenedione and testosterone to the aromatic estrogens estrone and estradiol, respectively. These endogenous hormones are a key factor in cancer tumor formation and proliferation through a cascade starting from estrogen binding to estrogen receptor. To interfere with the overproduction of estrogens especially in tumor tissue, it is possible to inhibit aromatase activity. This can be achieved using aromatase inhibitors. In order to design novel aromatase inhibitors, it is necessary to have an understanding of the active site of aromatase. As no crystal structure of the enzyme has yet been published, we built a homology model of aromatase using the first crystallized mammalian cytochrome enzyme, rabbit 21-progesterone hydroxylase 2C5, as a template structure. The initial model was validated with exhaustive molecular dynamics simulation with and without the natural substrate androstenedione. The resulting enzyme–substrate complex shows very good stability and only two of the residues are in disallowed regions in a Ramachandran plot.