[Enteral feeding therapy in patients with head and neck neoplasms].
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Enteral Nutrition↗
Biomedical subjects
V Müller
Publications and source records attributed to V Müller.
The karyotype of Trichobilharzia franki Müller et Kimmig, 1994 (Digenea:Schistosomatidae), a new European schistosome agent of swimmers' itch.
Chromosome characteristics of Trichobilharzia franki Müller et Kimming, 1994, causing swimmer's itch in the Western Germany, were described and compared with the karyotype of the sympatric species Trichobilharzia szidali Neuhaus, 1952. Karyotypes of both species are very similar: diploid sets consist of seven pairs of autosome chromosomes and one pair of sex chromosomes (2n = 16, n = 5m + 2sm + Zsm/Wst), the sex determining mechanism is ZZ in males and ZW in females and gross morphology of autosome pairs does not differ markedly. The only clear discriminative feature lies in the size and shape of sex chromosomes.
Animals↗
Probing the role of positive residues in the ADP/ATP carrier from yeast. The effect of six arginine mutations of oxidative phosphorylation and AAC expression.
ADP/ATP transport is the terminal step of oxidative phosphorylation in mitochondria. In this paper seven mutants of AAC2 from Saccharomyces cerevisiae are studied on the cellular and mitochondrial level. Six conspicuously located arginines were mutated into mostly neutral residues [Nelson, D. R., Lawson, J. E., Klingenberg, M., & Douglas, M. G. (1993) J. Mol. Biol. 230, 1159-1170]. R96A, R96H, R204L, and R294A are located in the second transmembrane helix of each repeat while R252I, R253I, and R254I are in the arginine triplet of the last domain. All six arginine residues are conserved in all known ADP/ATP carrier sequences. At the cellular level, oxidative phosphorylation in R96H and R294A retains 8% of the wild-type rate, but it is virtually zero in the other mutants. However, cytochrome c, a parameter of oxidative capacity, remains at 4-42% of wt. The weak coordination of respiratory chain and AAC expression indicates that respiration is needed also for other purposes. In mitochondria the AAC-linked ATP synthesis is measured and segregated by using the AAC inhibitor bongkrekate (BKA). Only the R96H and R294A mutants express a significant rate of AAC-dependent ATP synthesis amounting to 2-18% of the plasmid-borne wild-type AAC2 mitochondria. In all other mutants it is virtually zero. However, respiratory capacity and cytochrome c content are reduced only by 20-70%. Whereas in immunoblots the presence of AAC is detected in all mutant mitochondria, by quantitative ELISA no AAC can be measured down to 0.05 mumol of AAC dimer/g of protein in R96A and R204L, whereas in R96H, R2521, R2531, and R254I the content is around 0.2 and in R294A the content is 0.46 as compared to 0.6 in the plasmid wild type. Also the [3H]CAT and [3H]BKA binding is virtually zero in some mutants and closely parallels the ELISA-determined AAC content, indicating that the mutations did not affect the inhibitor binding site. The turnover of AAC [V(ATP)/AAC content] in oxidative phosphorylation is reduced to 10% or 20% except for the two intrahelical mutants R96H and R294A. In the three Arg triplet mutants, it is nearly zero. In conclusion, the first two intrahelical arginines R96 and R204, are essential for expression but probably also for the activity of AAC. R294A still retains good transport activity and remarkably high expression of AAC. All arginines in the triplet 252, 253, 254 are essential. Extrapolation of the in vitro phosphorylation rates to the cellular level by the cytochrome c factor reveals a large discrepancy to the in vivo rates in particular for R294A. This indicates that these mutations render the AAC more sensitive to the regulatory intracellular ATP/ADP ratio than the wt AAC.
Amino Acid Sequence↗
Probing the role of positive residues in the ADP/ATP carrier from yeast. The effect of six arginine mutations on transport and the four ATP versus ADP exchange modes.
Mutagenesis of three intrahelical arginines, R96, R204, or R294, and of each member of the arginine triplet R252, R253, R254 into neutral residues had resulted in a strong suppression of oxidative phosphorylation in cells and isolated mitochondria [Müller, V., Basset, G., Nelson, D. R., & Klingenberg, M. (1996) Biochemistry 35, 16132-16143]. Here we determine the transport activity of wild-type and mutant AAC in reconstituted proteoliposomes using a new rapid removal-stop method without relying on the inhibitor stop which can be compromised by mutations. The basic electroneutral ADP/ADP exchange activity is strongly or totally suppressed in six out of seven of these mutations, with the exception of R294A, which retains nearly wild-type activity. Carboxyatractylate (CAT) inhibits the ADP/ATP exchange rate only to 3-10% in wild type and R294A and up to 40% in other mutants, whereas bongkrekic acid (BKA) inhibits 50% (wild type and R294A) and 90% (other mutants). Consequently, AAC is preferentially reconstituted with the matrix surface outside. All these mutations drastically change activity distribution among the four exchange modes ADP/ADP, ADP/ATP, ATP/ADP, and ATP/ATP. Whereas in wild-type AAC the homo ATP/ATP exchange is twice as high as the ADP/ADP exchange, in mutants it is 10 to 15 times lower. Similarly, the hetero ATP/ADP exchange in wild-type AAC is higher than the ADP/ ATP exchange, but in mutants it is several times lower. Thus, these mutations afflict the ATP-linked modes, in particular those linked to external ATP. The inhibition of oxidative phosphorylation is thus explained by the suppression of ATP export versus ADP import mode. The "extra"-inhibition of oxidative phosphorylation in mutant cells is explained by the extreme shift in mutants in favour of ATP import versus ADP export. Besides structural changes, the mutant effects indicate electrostatic interactions of these arginines with the anionic substrates. The loss of one positive charge raises the translocation barrier the more negative the substrate, i.e. more for ATP4- than for ADP3-. In none of these arginine mutants was the binding of CAT or BKA abolished.
Arginine↗
Subunit structure and organization of the genes of the A1A0 ATPase from the Archaeon Methanosarcina mazei Gö1.
The proton-translocating A1A0 ATP synthase/hydrolase of Methanosarcina mazei Gö1 was purified and shown to consist of six subunits of molecular masses of 65, 49, 40, 36, 25, and 7 kDa. Electron microscopy revealed that this enzyme is organized in two domains, the hydrophilic A1 and the hydrophobic A0 domain, which are connected by a stalk. Genes coding for seven hydrophilic subunits were cloned and sequenced. From these data it is evident that the 65-, 49-, 40- and 25-kDa subunits are encoded by ahaA, ahaB, ahaC, and ahaD, respectively; they are part of the A1 domain or the stalk. In addition there are three more genes, ahaE, ahaF, and ahaG, encoding hydrophilic subunits, which were apparently lost during the purification of the protein. The A0 domain consists of at least the 7-kDa proteolipid and the 36-kDa subunit for which the genes have not yet been found. In summary, it is proposed that the A1A0 ATPase of Methanosarcina mazei Gö1 contains at least nine subunits, of which seven are located in A1 and/or the stalk and two in A0.
Amino Acid Sequence↗
Regulation and role of TGF beta production in breast cancer.
The influence of antiestrogens on the secretion of transforming growth factor beta (TGF beta) proteins that have an autoinhibitory potential for human cancer cells was studied in the estrogen-responsive human breast cancer cell line, MCF-7: Antiestrogens induce the secretion of TGF beta-1 via a nontranscriptional pathway; TGF beta-1 itself induces TGF beta-2 by a direct transcriptional mechanism; and TGF beta-2 is a marker of antiestrogen action. This hypothesis was confirmed in a clinical study with 18 patients with advanced metastatic breast cancer. TGF beta-2 plasma levels were measured before and after 4 weeks of treatment with tamoxifen. In the majority of patients who responded to the treatment, increasing TGF beta-2 concentrations were seen under therapy. Patients who did not respond did not show changes in the TGF beta-2 plasma level after 4 weeks of treatment. These results suggest that the sequential analysis of TGF beta-1 in plasma before and under treatment with tamoxifen allows the early identification of patients with antiestrogen resistance.
Breast Neoplasms↗
Z-DNA-forming sites within the human beta-globin gene cluster.
Agarose-encapsulated, metabolically active, permeabilized nuclei from human hematopoietic cell lines were tested for Z-DNA formation in the beta-globin gene cluster. Biotinylated monoclonal antibodies against Z-DNA were diffused into the nuclei and cross-linked to DNA with a 10-ns laser exposure at 266 nm. Following digestion with restriction enzymes, fragments that had formed Z-DNA were isolated. Seventeen regions with Z-DNA sequence motifs in the 73-kb region were studied by PCR amplification, and five were found in the Z conformation.
Cells, Cultured↗
P3 and contingent negative variation in Parkinson's disease.
Patients with idiopathic Parkinson's syndrome, most of them in early stages of the disease, and matched healthy controls participated in a continuous performance task while their EEGs were recorded from 15 electrodes. During preparation of movements, a contingent negative variation (CNV) maximal at central and posterior sites was visible. This CNV was reduced in the patient population. A large P3-like positive deflection occurred after go and no-go stimuli that called for execution (go) or suppression (no-go) of a button press. Compared to healthy controls, the positive wave in Parkinson patients was significantly reduced after go stimuli and maximally attenuated when no-go stimuli had indicated to suppress the motor response. In contrast, P3 amplitudes after irrelevant "ignore' stimuli was not significantly reduced in the patients. These results are interpreted in the framework of a model of striatal function postulating (i) that populations of cortical and striatal neurons form distributed functional units (Hebbian cell assemblies), and (ii) that mutual inhibition between such cortico-striatal cell assemblies is mediated by the neostriatum, the forebrain structure primarily affected in Parkinson's disease.
Behavior↗
Molecular cloning, expression and characterization of a recombinant glutathione S-transferase from Echinococcus multilocularis.
We report the identification and characterization of the first cestode glutathione S-transferase (GST) cDNA sequence. A fragment of an Echinococcus multilocularis glutathione S-transferase cDNA was isolated by the polymerase chain reaction. Subsequently, a Lambda zap cDNA library prepared from mRNA from protoscolices of E. multilocularis was screened with this PCR fragment. A complete cDNA clone was isolated and the nucleotide sequence determined. Analysis of the E. multilocularis GST-deduced amino acid sequence indicates that it is clearly related to the mammalian mu-class GSTs. The E. multilocularis GST cDNA was expressed in Escherichia coli, using a protocol designed to produce the native enzyme rather than a fusion protein. The 25.5-kDa enzyme subunit was purified to homogeneity using glutathione-sepharose chromatography. Gel filtration demonstrated that this GST is enzymatically active as a homodimer. The recombinant enzyme had conjugating activity with organic hydroperoxides and with members of the trans,trans-2,4 alkadienal and trans-2-alkenal series, which are secondary products of lipid peroxidation.
Amino Acid Sequence↗
The vasoconstrictor effects of L-NAME, a nitric oxide synthase inhibitor, in pregnant rabbits.
1. We have used anaesthetized, acutely instrumented non-pregnant (NP) and late pregnant (P) New Zealand white rabbits to examine the possible role of nitric oxide (NO) in the pregnancy-induced fall of vascular tone and arterial pressure. Systemic, renal and pulmonary vascular resistance, as well as plasma concentrations of cyclic GMP (PcGMP) were compared before and after the inhibition of NO synthesis by N(G)-nitro-L-arginine methyl ester (L-NAME). 2. P rabbits had lower baseline total peripheral resistance (TPR), mean arterial pressure (MAP) and higher PcGMP than NP controls (all P < 0.05 or less). L-NAME (1, 10, 50 mg kg1, i.v.) resulted in dose-dependent elevation of TPR in both groups. However, the absolute, as well as percentage increases in TPR were greater (P < 0.05) in NP than in P rabbits. 3. Cardiac output (CO) was reduced more (P < 0.01) by NO inhibition in NP than P rabbits. Therefore, despite the smaller increase in TPR, the elevation of MAP was greater (P < 0.001) in P than NP rabbits. After L-NAME, NP rabbits developed more severe bradycardia and a greater increase of pulmonary vascular resistance which might have contributed to the more pronounced reduction of CO. 4. PcGMP increased in both groups following L-NAME, but more (P < 0.01) in NP than P rabbits. 5. Infusion of acetylcholine (ACh, 0.02 micromol l-1 kg-1) reduced MAP and TPR more (both P < 0.05) in NP than P rabbits and L-NAME reduced the ACh-induced depressor response only in NP rabbits. 6. These results suggest that the low vascular tone and arterial pressure in pregnant rabbits is not mediated by NO.
Acetylcholine↗
[Army engagement in Croatia. Nursing in a field hospital].
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Croatia↗
A new interpretation of antiestrogen action.
Despite differences in their pharmacological behavior, type I and type II antiestrogens have certain important properties in common. Both differ from estradiol in that they enhance the immunoreactivity of estrogen receptors, apparently by inducing conformational change that exposes an additional epitope for a particular monoclonal antibody. Moreover, both types of antihormones not only compete with estradiol for its binding to the receptor but they also react with another domain not recognized by the hormone. The binding capacity for either type of antiestrogen is nearly twice that for estradiol, providing definitive evidence for the existence of specific antiestrogen-binding sites that are postulated to be important in antagonist action. These findings suggest a unified two-site model which helps explain how the same substance can be both an agonist and an antagonist; why there may be species variations in the agonist/antagonist relationship of type I compounds; and why type II agents show only antagonistic properties. It is suggested that interaction with secondary, antagonist-specific binding sites may provide a useful screen in the search for new and improved antihormonal agents.
Animals↗
The Na(+)-translocating ATPase of Acetobacterium woodii is a F1F0-type enzyme as deduced from the primary structure of its beta, gamma and epsilon subunits.
A 4.5 kbp EcoRI fragment hybridizing to a fragment of uncD (coding for subunit beta of F1F0-ATPases) was cloned from chromosomal DNA of Acetobacterium woodii. The nucleotide sequence was determined and revealed five open reading frames (ORF), four of which were identified to code for subunits of the Na(+)-ATPase. The deduced amino acid sequences of these ORF's are homologous to subunit alpha (partial coding sequence, C-terminal end), gamma, beta and epsilon of F1F0-ATPases from various organisms; furthermore, the organization of the genes in the order uncA (alpha), uncG (gamma), uncD (beta), uncC (epsilon) is identical to the structure of unc operon as present in most bacteria. Downstream of uncC is an ORF whose deduced amino acid sequence has 53% sequence homology to AlgD from Pseudomonas aeruginosa. The structure and organization of the unc genes are the final proof that the Na(+)-ATPase from A. woodii is a member of the family of F1F0-ATPases.
Acetobacter↗
Tumefactive megalocytic interstitial nephritis in a patient with Escherichia coli bacteremia.
Megalocytic interstitial nephritis is rare and primarily affects the cortex in an otherwise normal kidney. We recently encountered a patient with Escherichia coli bacteremia and oliguric acute renal failure who died of gram-negative septicemia. At autopsy, this patient's kidneys displayed typical features of megalocytic interstitial nephritis. We were able to perform special stains suggesting that the histiocytic interstitial cells originated from infiltrating macrophages. Our patient illustrates that macrophage proliferation can result in interstitial inflammation sufficiently severe to cause anuric acute renal failure.
Acute Kidney Injury↗
Partial orthotopic liver transplantation in rats.
A partial orthotopic liver transplantation technique (70% POLT) for use in rats and comparable with the corresponding recipient operation in the 'splitting transplantation' in man was developed. Body weight, liver function, histological and electron-microscopic findings were studied in comparison with whole rat liver transplantation with rearterialization, 30% POLT and corresponding liver resections. After 70 and 30% POLT typical signs of hepatic regeneration were found, but no pathological alterations in the electron-microscopic picture. This POLT model might be helpful for the investigation of unresolved questions in 'splitting transplantation'.
Animals↗
The carboxy-terminal F domain of the human estrogen receptor: role in the transcriptional activity of the receptor and the effectiveness of antiestrogens as estrogen antagonists.
Of the steroid hormone receptor family members, the estrogen receptor (ER) is notable in containing a sizable (42-amino acid) C-terminal region, denoted domain F. This F region differs from its adjacent hormone-binding domain, domain E, in that it is not well conserved among different vertebrate ER species, and its role in the biological activity of the ER is not well defined. We report an important role for the F domain of the ER in modulating the magnitude of gene transcription by estrogen and antiestrogen, and in determining the effectiveness of antiestrogens in suppressing estrogen-stimulated gene transcription. Using transient transfections, we have examined, in several cell types, the transcriptional activity of the full-length wild type human ER and ER lacking the carboxy-terminal F domain (delta F ER, containing amino acids 1-554) or ER altered in the F domain by point mutations. In some cells, namely Chinese hamster ovary (CHO) cells and MDA-MB-231 human breast cancer cells expressing wild type ER or delta F ER, estradiol (E2) stimulates equally transcription of several estrogen-responsive promoter-reporter gene constructs [estrogen ca-18119 element, (ERE)2-TATA-CAT, (ERE)2-pS2-CAT, (ERE)2-progesterone receptor(distal)-CAT]; however, the antiestrogens trans-hydroxytamoxifen and ICI 164,384, which stimulate transcription of some of these reporter constructs with the wild type ER, were unable to stimulate transcription with delta F ER. In addition, these antiestrogens were more effective antagonists of E2-stimulated transcription by delta F ER than by wild type ER. By contrast, in HeLa human cervical cancer cells and 3T3 mouse fibroblast cells, the delta F ER exposed to E2 is much less effective than wild type ER in stimulating transcription, and antiestrogens were less potent in suppressing E2-stimulated transcription by the delta F ER. These differences in response of the delta F and wild type ER to estrogen or antiestrogen do not appear to be due to a change in receptor expression level, binding affinity for ligands, or binding to estrogen response element DNA. Our data support the supposition that the conformation of the receptor-ligand complex is different with estrogen vs. antiestrogen and with wild type vs. delta F ER, such that its potential for interaction with protein cofactors or transcription factors is different and is markedly influenced by cell context. Thus, the F domain of the ER has a specific modulatory function that affects the agonist/antagonist effectiveness of antiestrogens and the transcriptional activity of the liganded ER in cells.
3T3 Cells↗
Purification of ATP synthase from Acetobacterium woodii and identification as a Na(+)-translocating F1F0-type enzyme.
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Amino Acid Sequence↗
The molecular structure of the Na(+)-translocating F1F0-ATPase of Acetobacterium woodii, as revealed by electron microscopy, resembles that of H(+)-translocating ATPases.
The Na(+)-translocating F1F0-ATPase of Acetobacterium woodii was examined by electron microscopy. After reconstitution into proteoliposomes, knobs typical for the F1 domain were visible on the outside of the membrane. The F1-part of the isolated enzyme showed a hexagonal symmetry suggesting an alpha 3 beta 3 structure, and the F1F0 complex had molecular dimensions very similar to those of H(+)-translocating ATPases of E. coli, chloroplasts, and mitochondria.
Adenosine Triphosphatases↗