Search

Objective: Between September, 2010, and August, 2011, a series of cases of jaundice of unknown origin in young calves was detected in a number of farms in Southern Germany. This paper describes the syndrome on the basis of 57 cases, and the approach taken to discover the cause. Material and methods: The clinical course of the disease is described in 19 patients. Using a case definition (calves aged 1–3 weeks, total serum bilirubin > 20 µmol/l and/or serum glutamate dehydrogenase [GLDH] activity >50U/l and/or autopsy findings with striking liver pathology [jaundice, liver dystrophy, cirrhosis]), 36 farms were included in an epidemiological survey. In a feeding trial, two batches of a dietary supplement feed, previously used in diseased calves on farms, were fed at the dosage recommendations of the manufacturer to four clinically healthy calves over 5days. Four other calves served as controls. The calves were clinically monitored daily, and blood samples were investigated using clinical chemistry and haematology. Results: Clinical examination revealed behavioural alterations (weakness, tonic-clonic seizures and bawling just before death), recumbency, jaundice and discolouration of faeces. In less severe cases without clinical signs, there was an increase in serum bilirubin concentration and/or GLDH activity. In the epidemiological survey of affected farms, the feeding of a diet supplement feed was registered in 54 of 57 cases. The feeding of two batches of that diet supplement feed to four clinically healthy calves resulted in a significant (p<0.05) increase in bilirubin and lactate concentrations, as well as the GLDH activity in serum, but without serious impairment of the general condition, whereas in control calves, no comparable changes were observed. Conclusion: The results of the epidemiological survey and the feeding trial suggest a causal involvement of a dietary supplement feed. The toxic principle is unknown. Clinical relevance: Knowledge of the clinical picture and the probable feed-related context is important to detect this disease early. The suspected dietary supplement feed has been taken off the market, but with other products similar problems may arise.

Bei der Verdichtung von Luft mithilfe von Kompressoren werden häufig unbeabsichtigt Ölaerosole freigesetzt. Die Massenkonzentration solcher Aerosole in der erzeugten Druckluft muss regelmäßig überprüft werden, insbesondere wenn die Druckluft für Beatmungszwecke verwendet wird, da das Ölaerosol gesundheitsschädlich ist. Bisher wurden solche Messungen mithilfe der Röhrchenmethode durchgeführt, die auf der Oxidation des Öls durch Schwefelsäure beruht. Nachteilig an der Röhrchenmethode ist aber, dass die erhaltenen Messergebnisse von der Ölsorte abhängig sind. Um diese Problematik zu vermeiden, wurde eine alternative Messmethode auf Basis eines Impaktors entwickelt, bei der es sich um eine rein mechanische Methode zur Abtrennung des Ölaerosols aus der Druckluft handelt. Im Rahmen des vorliegenden Artikels wird die Impaktormethode vorgestellt. Darüber hinaus werden Ergebnisse aus Untersuchungen mit dem Impaktor zu Öltröpfchengrößenverteilungen und zum Ölabscheidegrad dargelegt. Schließlich wird eine Methode zur Kalibrierung der Messung mit dem Impaktor beschrieben und die Anwendung der Impaktormethode in der Praxis diskutiert.

Crystallographic nets are defined. It is shown how these nets can be generated from finite graphs which are called the quotient graphs of the nets. The procedure yields the topology of the nets, their crystallographic point groups and their lattice types. (© 2004 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

Logistic regression models were used to examine the relationship between milk yield and incidence of certain disorders. Lactations (n=2197) of 1074 Holstein-Friesian cows from 10 dairies (25 to 146 cows per dairy) in Lower Saxony were studied. The 305-d yield from the previous and current lactations served as the standards for milk yield. Eight disorder complexes were considered: retained placenta, metritis, ovarian cysts, mastitis, claw diseases, milk fever, ketosis, and displaced abomasum. Each disorder complex was modeled separately. In addition to milk yield, the influences of the lactation number, the calving season and the other disorder complexes were examined with the “herd” factor taken into account. A correlation between retained placenta, mastitis, and milk fever to milk yield during the previous lactation was found to be probable and for ketosis and displaced abomasum such a correlation was found to be possible. A connection to the yield in the current lactation was shown for ovarian cysts, claw diseases, and milk fever. No relationship to milk yield existed for metritis. An influence of the lactation number was also demonstrated in various models. Single models allowed a demonstration of the influences of both milk yield and lactation number. Limitations of the model types are discussed.

Exposure of andalusite and kyanite powders (?40 µm) to high dynamic pressures revealed a strongly different behaviour of the two materials against shock. While experiments on andalusite powders yielded characteristic shock-induced phase transformations, kyanite powders did not show any phase change upon release from shock compression. X-ray patterns and infra-red spectra proved the formation of 3/2-mullite from andalusite, and infra-red spectra also indicated the formation of long-range-disordered Al2O3 and SiO2. While the formation of mullite must be associated with high (shock) temperatures, the formation of the Al2O3 + SiO2 oxide mixture may be a (shock) pressure effect. The lack of temperature-induced transformations in kyanite may be explained by the lower porosity of the sample tablets as compared to those of andalusite. The absence of highpressure transformations in kyanite is most probably due to its dense structure which is more resistant to shock waves than the more open andalusite structure.

Opiates and opioid peptides inhibit adenylate cyclase and stimulate specific low Km GTPase activity in membranes from neuroblastoma x glioma NG108-15 hybrid cells. The effects of opiate agonists on both enzymes are mediated by high affinity stereospecific receptors and require Mg2+, GTP, and Na+. In the presence of Mg2+, Na+ inhibits basal GTPase activity; opiates stimulate GTP hydrolysis by antagonizing the Na+-induced inhibition. Activation of GTPase leads, in turn, to inactivation of GTP-stimulated adenylate cyclase activity. The intrinsic activities (or efficacies) of a series of opiates are identical for stimulation of GTPase and inhibition of adenylate cyclase. These results provide a mechanism for the dual requirement for Na+ and GTP in the inhibitory coupling of opiate receptors to the adenylate cyclase system in these cells and may be of general significance to the action of other inhibitory hormones.

For the mineral fluorapatite, Ca10(PO4)6F2, a potential model of the polarizable ion type has been developed in order to reproduce the following physical constants: the vibrational frequencies (transverse and longitudinal), the elastic constants and the static and high frequency dielectric constants. The parameters of the model are short range force constants, ionic charges and ionic polarizabilities.

Receptors that reversibly bind opiates and opioid peptides have been solubilized from brain and neuroblastoma-glioma hybrid cell NG108-15 membranes. Active receptors are specifically solubilized with a new type of detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, which is a zwitterionic derivative of cholic acid. The solubilized receptor complexes behave as large molecules with a Stokes radius of 70 A and contain protein as an essential constituent.

We immunized rabbits with purified guanine nucleotide-binding proteins (G proteins) from bovine brain and obtained an antiserum, RV3, that reacts specifically with the alpha subunit (39 kDa) of a G protein of unknown function, termed Go, as well as with the beta subunit (35 kDa) common to all G proteins. RV3 showed no crossreactivity with the alpha subunits of the stimulatory (Gs) or inhibitory (Gi) G proteins associated with adenylate cyclase, nor with that of the rod outer segment G protein, transducin. Immunoblots with crude and affinity-purified antiserum showed that RV3 specifically recognizes the Go alpha subunit and the beta subunit in crude brain membranes. Using RV3, we found approximately equal amounts of Go in brain membranes from frog, chicken, rat, cow, and man. Quantitative immunoblotting gave Go alpha subunit/ beta subunit ratios approximately equal to 1 in cerebral cortex, raising the possibility that free Go alpha subunit (unassociated with beta subunit) may exist in brain. The concentration of Go alpha subunit in cortex is about 5 times that of Gi alpha subunit. The results show that Go is an immunochemically distinct, highly conserved protein distributed throughout the brain, with particularly high concentrations in forebrain.

We show that every doubly periodic planar map is isomorphic to one whose countries are convex, and that the corresponding statement is false in higher dimensions.

We tested 18 antisera showing reactivity against the alpha subunit of transducin, the guanine nucleotide binding protein from rod outer segment, for crossreactivity against the 40- and 39-kDa guanine nucleotide binding proteins purified from bovine brain. A single antiserum, CW6, showed crossreactivity, and this was predominantly against the 40-kDa protein. Immunoblots of the tryptic fragments of transducin alpha subunit with multiple antisera raised against that subunit showed that only CW6 recognizes a COOH-terminal 5-kDa peptide that includes the site of pertussis toxin ADP-ribosylation. Antibodies against the 5-kDa peptide, affinity-purified from CW6, specifically react with the 40-kDa brain protein on immunoblots. The results show that the 39- and 40-kDa guanine nucleotide binding proteins from brain differ immunochemically and that the COOH-terminal 5-kDa peptide of transducin alpha subunit is homologous to a region in the 40-kDa brain protein. We speculate that this homologous region may be in a domain that confers specificity for receptor interactions of guanine nucleotide binding proteins.

Using modifications of the methods of Bokoch et al. (Bokoch, G.M., Katada, T., Northup, J. K., Ui, M., and Gilman, A. G. (1984) J. Biol. Chem. 259, 3560-3567) and Codina et al. (Codina, J., Hildebrandt, J. D., Sekura, R. D., Birnbaumer, M., Bryan, J., Manclark, C. R., Iyengar, R., and Birnbaumer, L. (1984) J. Biol. Chem. 259, 5871-5886), we have purified a pertussis toxin substrate with the expected characteristics of the inhibitory guanine nucleotide-binding protein (Ni) essentially to homogeneity. The purified protein consists of 3 subunits of Mr 40,000, 35,000, and less than 10,000. The Mr 40,000 band is found, upon close examination, to consist of a poorly resolved doublet. Starting with the membranes from 1,320 g of bovine forebrain we purified the protein some 100-fold with approximately 20% yield to obtain 13 mg of a greater than 95% pure protein. Chromatography on octyl-Sepharose provided efficient separation of Ni from Ns (the stimulatory guanine nucleotide-binding protein). Analytical ultracentrifugation indicates an Mr of 82,000 and a sedimentation coefficient S20,w of 5.1. The protein is able to restore opiate-mediated inhibition of adenylate cyclase to membranes prepared from NG 108-15 cells which had been treated with pertussis toxin. Bovine brain Ni has the enzymatic properties of a low Km GTPase with a turnover number of 0.3 and affinities for nucleotides in the order GppNHp greater than or equal to GTP greater than or equal to GDP much greater than ATP, CTP, UTP, and GMP. Na+ specifically stimulates the GTPase and low concentrations of Mg2+ (less than 50 microM) are inhibitory. Some Mg2+ is apparently necessary because EDTA, but not EGTA, abolishes the GTPase activity.

The mu and delta opiate receptors present in rat brain were measured independently during postnatal development. The numbers of delta receptors were almost undetectable at birth and increased substantially during the first few weeks, whereas the numbers of mu receptors remained relatively constant. Activation of either of these receptors caused inhibition of adenylate cyclase, but inhibition coupled to mu receptors was much smaller than that associated with delta receptors at all ages. Attempts to use pertussis toxin-catalyzed ADP-ribosylation as an assay for the GTP-binding proteins Ni and No were hampered by the development of an NADase with age. However, specific antibodies directed against the alpha subunits of Ni or No allowed separate quantitation of these transducer proteins. Both increased with age. No is present at levels at least 5-fold higher than Ni in the adult rat brain. The N proteins are in vast excess over receptors and as such are unlikely to be limiting factors in receptor function. The data further suggest that the number of opiate receptors present throughout neonatal development is in excess over that required for optimal function.

Morphine inhibits adenylate cyclase (EC 4.6.1.1) activity of neuroblastoma times glioma hybrid cells. The inhibition is stereospecific and is reversed by the antagonist, naloxone. The relative affinities of narcotics for the opiate receptor agree well with their effectiveness as inhibitors of adenylate cyclase. Morphine-sensitive and -insensitive cell lines were found, and the degree of sensitivity was shown to be dependent upon the abundance of narcotic receptors. Thus, morphine receptors are functionally coupled to adenylate cyclase. A molecular mechanism for narcotic addiction and tolerance is proposed.

Photolabile derivatives of D-Ala2-Leu5-enkephalin were prepared by synthetic procedures in which a 2-nitro-4-azidophenyl group is linked to the terminal carboxyl group of the enkephalin by means of an ethylenediamine or ethylenediamine beta-alanine spacer. These peptides bind to opiate receptors with nanomolar affinities and inhibit electrically stimulated contractions of the mouse vas deferens and adenylate cyclase activity of NG108-15 neuroblastoma x glioma hybrid cell membranes. Both inhibitions are reversed by the opiate antagonist naloxone. Photolysis of the ligands bound to rat brain membranes results in the loss of approximately 50% of the receptor sites. This decrease in receptor number is blocked by naloxone and requires light. A photolabile [3H]enkephalin derivative labels an equivalent number of sites under similar irradiation conditions.

Narcotics affect adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] in two opposing ways, both mediated by the opiate receptor. The first process is the readily reversible inhibition of the enzyme by narcotics; the second is a compensatory increase in enzyme activity which is delayed in onset and relatively stable. Late positive regulation of the enzyme counteracts the inhibitory influence of morphine and is responsible for narcotic dependence and tolerance. The coupled inhibitory and positive regulatory mechanisms for adenylate cyclase provide a means of activating and deactivating neural circuits hours after the initial event and thus may play a role in a memory process.

Tissue samples from the feet of slaughtered cattle exhibiting different stages of digital dermatitis were sectioned and stained with haematoxylin and eosin and silver staining techniques. Three morphological variations of spirochaetes were observed, whereas control samples from feet which were macroscopically negative for digital dermatitis were also negative for spirochaetes. In an immunofluorescence test, [i]Campylobacter faecalis[/i] was found to be abundant on superficial wound smears from the classical ulceration of digital dermatitis.

The delta opiate receptor gene has been cloned from the mouse neuroblastoma-rat glioma hybrid cell NG108-15. The clone that we isolated is apparently identical to that reported by Evans et al. [Evans, C. J., Keith, D. E., Jr., Morrison, H., Magendzo, K. & Edwards, R. H. (1992) Science 258, 1952-1955] and essentially identical with that of Kieffer et al. [Kieffer, B. L., Befort, K., Gaveriaux-Ruff, C. & Hirth, C. G. (1992) Proc. Natl. Acad. Sci. USA 89, 12048-12052]. We have found full-length transcripts of the gene in mouse brain but in no other tissues examined. Within the brain the gene is expressed at low levels in many regions but transcripts are found in particularly large amounts in the anterior pituitary and pineal glands. Since these tissues are located outside the blood-brain barrier, opioid peptides easily can reach receptors in these areas from the blood. The gene, which is present as a single copy, has been mapped to the distal region of mouse Chromosome 4.

The addition of bradykinin to NG108-15 cells results in a transient hyperpolarization followed by prolonged cell depolarization. Injection of inositol 1,4,5-trisphosphate or Ca2+ into the cytoplasm of NG108-15 cells also elicits cell hyperpolarization followed by depolarization. Tetraethylammonium ions inhibit the hyperpolarizing response of cells to bradykinin or inositol 1,4,5-trisphosphate. Thus, the hyperpolarizing phase of the cell response may be due to inositol 1,4,5-trisphosphate-dependent release of stored Ca2+ into the cytoplasm, which activates Ca2+-dependent K+ channels. The depolarizing phase of the cell response to bradykinin is due largely to inhibition of M channels, thereby decreasing the rate of K+ efflux from cells and, to a lesser extent, to activation of Ca2+-dependent ion channels and Ca2+ channels. In contrast, injection of inositol 1,4,5-trisphosphate or Ca2+ into the cytosol did not alter M channel activity. Incubation of NG108-15 cells with pertussis toxin inhibits bradykinin-dependent cell hyperpolarization and depolarization. Bradykinin stimulates low Km GTPase activity and inhibits adenylate cyclase in NG108-15 membrane preparations but not in membranes prepared from cells treated with pertussis toxin. Reconstitution of NG108-15 membranes from cells treated with pertussis toxin with nanomolar concentrations of a mixture of highly purified No and Ni [guanine nucleotide-binding proteins that have no known function (No) or inhibit adenylate cyclase (Ni)] restores bradykinin-dependent activation of GTPase and inhibition of adenylate cyclase. These results show that [bradykinin . receptor] complexes interact with No or Ni and suggest that No and/or Ni mediate the transduction of signals from bradykinin receptors to phospholipase C and adenylate cyclase.

Specific, GTP hydrolysis catalyzed by membranes prepared from neuroblastoma--glioma (NG108-15) hybrid cells can be measured in the presence of adenosine-5'-[beta, gamma-imido] triphosphate (p[NH]ppA), ATP, and a nucleotide triphosphate-regenerating system. Opiates and opioid peptides stimulate low Km GTP hydrolysis when measured in the presence of Na+ and Mg2+. Opiate stimulation is rapid, stereospecific, and reserved by the antagonist naloxone. Potencies of opiates as stimulators of GTP hydrolysis and as inhibitors of adenylate cyclase are closely correlated. Agents that stimulate adenylate cyclase, including prostaglandin E1, 2-Cl-adenosine, secretin, and NaF, have little or no effect upon the rate of GTP hydrolysis. Opiates have no effect upon either adenylate cyclase or GTPase activity in membranes prepared from C6-BU1 glioma cells, which lack opiate receptors. In view of the pivotal role of GTP in the activation of adenylate cyclase, we conclude that receptor-mediated stimulation of GTP hydrolysis is the mechanism by which opiates and other inhibitory hormones lower adenylate cyclase activity in NG108-15 cell membranes.

Reactions mediated by the opiate receptors that inhibit adenylate cyclase (EC 4.6.1.1) are closely coupled to subsequent reactions that gradually increase adenylate cyclase activity of neuroblastoma X glioma NG108-15 hybrid cells. Opiate-treated cells have higher basal-, prostaglandin E1-, and 2-chloroadenosine-stimulated activities than do control cells. However, NaF or guanosine 5'-(beta, gamma-imido)triphosphate abolishes most of the differences in adenylate cyclase activity observed with homogenates from control and opiate-treated cells. Cycloheximide blocked some, but not all, of the opiate-dependent increase in adenylate cyclase activity. These results suggest that the opiate-dependent increase in adenylate cyclase is due to conversion of adenylate cyclase to a form with altered activity. Protein synthesis also is required for part of the opiate effect. We propose that activity of adenylate cyclase determines the rate of conversion of the enzyme from one form to the other and that opiates, by inhibiting adenylate cyclase, alter the relative abundance of low- and high-activity forms of the enzyme.

Opiate receptors from NG108-15 neuroblastoma-glioma hybrid cell membranes were purified to apparent homogeneity in a form covalently labeled with the opiate affinity ligand 3-methylfentanylisothiocyanate (super-FIT). The purification procedure consists of five steps: quantitative labeling of opiate receptors in membranes with super-FIT; solubilization in a lubrol/3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate mixture; adsorption to and elution from a wheat germ agglutinin-Sepharose column; immunoaffinity chromatography on columns of immobilized anti-fentanyl; preparative gel electrophoresis in the presence of NaDodSO4. The protein was purified approximately 30,000-fold in 3% overall yield to a state in which there is 1 mol of super-FIT bound per mol of protein, corresponding to 21,000 pmol per mg of protein, the theoretically expected specific activity. The protein is glycosylated and migrates on NaDodSO4 gel electrophoresis with a Mr near 58,000. It has a strong tendency to dimerize, even in the presence of denaturing detergents, and it exists primarily as an oligomer in nondenaturing detergents.

Several letters to the editor are presented in response to articles in previous issues including "Classical Look at the 'Real Cost' of Money" in the June 28, 1969 issue, "Why Northwest Puts on the Ritz" in the July 5, 1969 issue, and "What's Wrong at Chrysler" in the July 5, 1969 issue.

Visual examination, electron-microscopic observation and infrared-spectroscopic analysis demonstrate that the thermodynamically unstable calcium oxalate trihydrate, which supposedly plays an important role in the formation of certain urinary calculi, is a commonly occurring constituent of urinary stones.

Incubation of neuroblastoma X glioma hybrid cells for 12-97 hr with methionine-enkephalin results in an increase in adenylate cyclase activity [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] that is mediated by the opiate receptor. The results show that cells become tolerant to, and dependent upon, enkephalin.

Summary Pure cholesterolgallstones can be diBolved by chenodesoxycholic acid (CDC). The composition of 208 gallstones was examined: 93.7% contained cholesterol, but only 10.6% were pure cholesterol stones. Radiologically no differentiation between pure cholesterolgallstones and mixed stones with a low calcium content was poBible. With CDC there is an increase of liver enzymes, choleraic diarrhea, and hepatotoxic lithocholic acid. As a rule, recurrent stones are observed after discontinued treatment with CDC.