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H Schmidt

Publications and source records attributed to H Schmidt.

At least 361 records · Page 20Linked to original sources

Design of a multiple slice interface chamber and application for resolving the temporal pattern of CREB phosphorylation in hippocampal long-term potentiation.

We describe an improved method for the investigation of time-dependent intracellular events giving rise to long-lasting changes in synaptic efficacy. A new interface chamber for the simultaneous superfusion of approximately 30 rat hippocampal slices was designed. The slice chamber contains an upper and a lower medium reservoir connected by a grooved incubation platform which is mounted at an angle of 7 degrees on a thermoregulation unit. Surface slices placed in the chamber are perfused with oxygenated medium at a rate of 1 ml/min and are maintained synaptically viable for at least 6 h. At different time points after induction of long-term potentiation by stimulation of the Schaffer collateral pathway, slices were either fixed in Zamboni's fixative or the CA1 region was excised and lysed in boiling SDS-sample buffer. Fixed 400 microm hippocampal slices were cut into 30 microm sections and immunocytochemically stained with an anti-serine 133 phosphorylated cAMP-responsive element binding protein (pCREB) antibody. Binding of primary antibody was detected with the avidin-biotinylated peroxidase complex method and enhanced using peroxidase-catalyzed deposition of biotinylated tyramine. Staining was visualized with streptavidin-cyanine 3.18 and observed under a confocal laser scanning microscope. CA1 lysates were electrophoresed and subjected to Western blot analysis. Both pCREB immunocytochemical staining and Western blotting showed that CREB is rapidly and transiently phosphorylated after induction of long-term potentiation. pCREB levels peaked within 30 min and declined back to control after 60 min. Immunocytochemistry also showed that pCREB was localized to the nuclei of CA1 pyramidal cells near the tetanization site.

Animals↗

Perillic acid inhibits Ras/MAP kinase-driven IL-2 production in human T lymphocytes.

Perillic acid, a major metabolite of d-limonene, substantially suppressed interleukin-2 (IL-2) and IL-10 production in mitogen-activated T lymphocytes. The effects of perillic acid on cytokine secretion were selective: IL-6 and transforming growth factor-beta 1 (TGF-beta 1) generation were unchanged. In H9 T lymphoma cells, exposure to perillic acid resulted in a dose-dependent depletion of membrane-bound Ras proteins. Unlike hydroxymethyl-glutaryl-CoA reductase or protein farnesyltransferase inhibitors, perillic acid did not induce a shift of membrane-bound into cytosolic p21ras but depleted total cellular Ras proteins. Triggering of the T cell receptor (TCR) perturbs the guanine nucleotide binding cycle of p21ras and in turn induces phosphorylation and activation of mitogen-activated protein kinases (MAPK). In perillic acid-treated cells, the levels of phosphorylated but not total MAPK were also decreased in a dose-dependent manner. Taken together, we provide evidence that perillic acid interrupts signalling via the Ras/MAP kinase pathway by depleting farnesylated Ras levels, an effect which may contribute to its inhibition of IL-2 production and T cell activation.

Calcium-Calmodulin-Dependent Protein Kinases↗

Interferon gamma gene expression in sensory neurons: evidence for autocrine gene regulation.

We explored expression and possible function of interferon-gamma (IFN-gamma) in cultured fetal (E15) rat dorsal root ganglion neurons combining whole cell patch-clamp electrophysiology with single cell reverse transcriptase polymerase chain reaction and confocal laser immunocytochemistry. Morphologically, we located IFN-gamma protein in the cytoplasm of the neurons in culture as well as in situ during peri- and postnatal development. Transcripts for classic IFN-gamma and for its receptor were determined in probes of cytoplasm sampled from individual cultured neurons, which had been identified by patch clamp electrophysiology. In addition, the cultured neurons expressed both chains of the IFN-gamma receptor. Locally produced IFN-gamma acts back on its cellular source. Phosphorylation and nuclear translocation of the IFN-inducible transcriptional factor STAT1 as well as IFN-gamma-dependent expression of major histocompatibility complex class I molecules on the neuronal membrane were noted in untreated cultures. However, both processes were substantially blocked in the presence of antibodies neutralizing IFN-gamma. Our findings indicate a role of IFN-gamma in autocrine regulation of sensory neurons.

Animals↗

Central nervous system TNFalpha-mRNA expression during rabbit experimental pneumococcal meningitis.

In pneumococcal meningitis inflammatory mediators such as tumor necrosis factor alpha (TNFalpha) are produced in large quantities and play a major role in pathogenesis. It is not known exactly which cells produce these mediators during infection. We investigated the localisation of TNFalpha-mRNA in the central nervous system (CNS) by in situ hybridisation during experimental Streptococcus pneumoniae meningitis. TNF-positive cells were detected only in inflammatory infiltrates within the meninges. Cells within the brain parenchyma and the choroid plexus were completely negative. After monocyte depletion, no TNFalpha-mRNA positive cells were detected in the CNS. These findings suggest that TNFalpha in pneumococcal meningitis is produced in the CNS mainly by blood-derived, infiltrating monocytes.

Animals↗

Risk factors for microangiopathy-related cerebral damage in the Austrian stroke prevention study.

Microangiopathy-related cerebral damage (MARCD) represents a common incidental MRI observation in the elderly. The risk factors of such findings are widely unknown. We therefore performed MRI in 349 randomly selected volunteers (ages 50 to 70 years) without neuropsychiatric disease, and evaluated the association of MARCD with conventional and recently suggested cerebrovascular risk factors such as apolipoprotein E genotypes, plasma concentrations of essential antioxidants and anticardiolipin antibody titres. MARCD was defined as evidence of early confluent and confluent deep white matter hyperintensities and lacunes. It was present in 71 (20.3%) subjects. Individuals with MARCD were older than those without such findings (62.7 years vs 59.6 years; P=0.0001). They had a higher rate of arterial hypertension (45.1% vs 28.1%; P=0.006) and cardiac disease (50.7% vs 37.1%; P=0.04), higher systolic blood pressure readings at exam (144.4 mmHg vs 136.7 mmHg; P=0.004), and higher serum fibrinogen concentrations (327.1 mg/dl vs 292.5 mg/dl; P=0.001). Their levels of total cholesterol (217.6 mg/dl vs 231.2; P=0.009), apolipoprotein A-I (167.3 mg/dl vs 177.4 mg/dl, P=0.02), lycopene (0.17 micromol/l vs 0.24 micromol/l; P=0.003), retinol (1.91 micromol/l vs 2.10 micromol/l; P=0.02) and alpha-tocopherol (27.55 micromol/l vs 31.14 micromol/l; P=0.001) were significantly lower. Forward stepwise regression analysis created a model of independent predictors of MARCD with age entering first (odds ratio 2.01/10 years), fibrinogen second (odds ratio 2.45/100 mg/dl), alpha-tocopherol third (odds ratio 0.55/10 micromol/l), and arterial hypertension fourth (odds ratio 1.96). The association of MARCD with various treatable clinical conditions may have preventive implications.

Aged↗

The embryonic central nervous system lineages of Drosophila melanogaster. II. Neuroblast lineages derived from the dorsal part of the neuroectoderm.

In Drosophila, central nervous system (CNS) formation starts with the delamination from the neuroectoderm of about 30 neuroblasts (NBs) per hemisegment. They give rise to approximately 350 neurons and 30 glial cells during embryonic development. Understanding the mechanisms leading to cell fate specification and differentiation in the CNS requires the identification of the NB lineages. The embryonic lineages derived from 17 NBs of the ventral part of the neuroectoderm have previously been described (Bossing et al., 1996). Here we present 13 lineages derived from the dorsal part of the neuroectoderm and we assign 12 of them to identified NBs. Together, the 13 lineages comprise approximately 120 neurons and 22 to 27 glial cells which we include in a systematic terminology. Therefore, NBs from the dorsal neuroectoderm produce about 90% of the glial cells in the embryonic ventral ganglion. Two of the NBs give rise to glial progeny exclusively (NB 6-4A, GP) and five to glia as well as neurons (NBs 1-3, 2-5, 5-6, 6-4T, 7-4). These seven NBs are arranged as a group in the most lateral region of the NB layer. The other lineages (NBs 2-4, 3-3, 3-5, 4-3, 4-4, 5-4, clone y) are composed exclusively of neurons (interneurons, motoneurons, or both). Additionally, it has been possible to link the lateral cluster of even-skipped expressing cells (EL) to the lineage of NB 3-3. Along with the previously described clones, the vast majority (more than 90%) of cell lineages in the embryonic ventral nerve cord (thorax, abdomen) are now known. Moreover, previously identified neurons and most glial cells are now linked to certain lineages and, thus, to particular NBs. This complete set of data provides a foundation for the interpretation of mutant phenotypes and for future investigations on cell fate specification and differentiation.

Animals↗

Intestinal formation of hypoxanthine and uric acid during endotoxemia.

The objective of this study was to examine the intestinal metabolism of high-energy purine compounds as sensitive indicators of tissue ischemia during endotoxemia. Arterial (art) and portal venous (PV) concentrations as well as the intestinal net concentration changes of adenosine (ADO), hypoxanthine (Hypo), and uric acid (UA) were measured at baseline and after 60 and 120 min in rats that were subjected to a 1-hr continuous infusion of endotoxin (1.5 mg/kg; group E), and in control animals (group C). Furthermore, the arterial (SaO2) and portal venous oxygen saturation (S(PV)O2) was determined at the same time points. Animals in both groups remained normotensive throughout the study period and no differences in mean arterial blood pressure were observed. In both groups, adenosine concentrations remained constant throughout the study and no changes in the net concentration difference (NCD) of adenosine between arterial and portal venous blood were observed [ADO(NCD); baseline: group E, -23 +/- 46 nmole/L; group C, 17 +/- 84 nmole/L; 120 min: group E, 14 +/- 38 nmole/L; group C, 5 +/- 40 nmole/L]. In contrast to control animals, hypoxanthine and uric acid concentrations increased in arterial and portal venous blood in endotoxemic rats after 120 min. This was accompanied with an increase in the intestinal net concentration differences of both hypoxanthine and uric acid, indicating the gut as the predominant source of these two compounds during endotoxemia [Hypo(NCD); baseline: group E, -36 +/- 53 nmole/L; group C, -53 +/- 185 nmole/L; 120 min: group E, 538 +/- 211 nmole/L; group C, 99 +/- 100 nmole/L] [UA(NCD); baseline: group E, 2.04 +/- 1.62 micromole/L; group C, -0.04 +/- 1.11 micromole/L; 120 min: group E, 9.58 +/- 3.04 micromole/L; group C, 0.35 +/- 1.34 micromole/L]. Furthermore, in endotoxemic rats the portal venous oxygen saturation decreased despite unaltered arterial oxygen saturation [SaO2; baseline: group E, 95.2 +/- 0.9%; group C, 94.2 +/- 0.9%; 120 min: group E, 95.4 +/- 0.7%; group C, 96.4 +/- 0.9%] [S(PV)O2; baseline: group E, 86.2 +/- 3.1%; group C, 85.7 +/- 1.4%; 120 min: group E, 69.1 +/- 4.5%; group C, 82.3 +/- 1.9%]. These results indicate the presence of tissue ischemia in the intestinal tract during early, normotensive endotoxemia. Furthermore, because of the direct toxic damage mediated by oxygen radicals that are generated during the production of uric acid, intestinal mucosal injury observed during endotoxemia may be related to an enhancement of the ATP-degradation pathway.

Adenosine↗

Complementation of the DNA repair-deficient swi10 mutant of fission yeast by the human ERCC1 gene.

In human cells DNA damage caused by UV light is mainly repaired by the nucleotide excision repair pathway. This mechanism involves dual incisions on both sides of the damage catalyzed by two nucleases. In mammalian cells XPG cleaves 3' of the DNA lesion while the ERCC1-XPF complex makes the 5' incision. The amino acid sequence of the human excision repair protein ERCC1 is homologous with the fission yeast Swi10 protein. In order to test whether these proteins are functional homologues, we overexpressed the human gene in a Schizosaccharomyces pombe swi10 mutant. A swi10 mutation has a pleiotropic effect: it reduces the frequency of mating type switching (a mitotic transposition event from a silent cassette into the expression site) and causes increased UV sensitivity. We found that the full-length ERCC1 gene only complements the transposition defect of the fission yeast mutant, while a C-terminal truncated ERCC1 protein also restores the DNA repair capacity of the yeast cells. Using the two-hybrid system of Saccharomyces cerevisiae we show that only the truncated human ERCC1 protein is able to interact with the S . pombe Rad16 protein, which is the fission yeast homologue of human XPF. This is the first example yet known that a human gene can correct a yeast mutation in nucleotide excision repair.

Adenosine Triphosphatases↗

Mössbauer studies of alkane omega-hydroxylase: evidence for a diiron cluster in an integral-membrane enzyme.

The gene encoding the alkane omega-hydroxylase (AlkB; EC 1.14.15.3) from Pseudomonas oleovorans was expressed in Escherichia coli. The integral-membrane protein was purified as nearly homogeneous protein vesicles by differential ultracentrifugation and HPLC cation exchange chromatography without the detergent solubilization normally required for membrane proteins. Purified AlkB had specific activity of up to 5 units/mg for octane-dependent NADPH consumption. Mössbauer studies of AlkB showed that it contains an exchange-coupled dinuclear iron cluster of the type found in soluble diiron proteins such as hemerythrin, ribonucleotide reductase, methane monooxygenase, stearoyl-acyl carrier protein (ACP) delta9 desaturase, rubrerythrin, and purple acid phosphatase. In the as-isolated enzyme, the cluster contains an antiferromagnetically coupled pair of high-spin Fe(III) sites, with an occupancy of up to 0.9 cluster per AlkB. The diferric cluster could be reduced by sodium dithionite, and the diferrous state was found to be stable in air. When both O2 and substrate (octane) were added, however, the diferrous cluster was quantitatively reoxidized, proving that the diiron cluster occupies the active site. Mossbauer data on reduced AlkB are consistent with a cluster coordination rich in nitrogen-containing ligands. New sequence analyses indicate that at least 11 nonheme integral-membrane enzymes, including AlkB, contain the 8-histidine motif required for catalytic activity in stearoyl-CoA desaturase. Based on our Mössbauer studies of AlkB, we propose that the integral-membrane enzymes in this family contain diiron clusters. Because these enzymes catalyze a diverse range of oxygenation reactions, this proposal suggests a greatly expanded role for diiron clusters in O2-activation biochemistry.

Iron↗

An ileX tRNA gene is located close to the Shiga toxin II operon in enterohemorrhagic Escherichia coli O157 and non-O157 strains.

A cosmid library of enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain EDL 933 was constructed and clones carrying the stx2 gene were identified by colony blot hybridization with a stx2B specific probe. Nucleotide sequencing upstream of the stx2A gene revealed high sequence identities of 89.5% to the ileX tRNA gene found in E. coli. The ileX gene was located 260 bp from the translational start codon of stx2A. PCR analysis with primers specific for this analyzed region showed that in 11 Stx2-producing EHEC strains from patients with hemolytic uremic syndrome, all PCR-positive strains carried the ileX tRNA gene. However, PCR analysis of the respective region in 11 Stxl-producing EHEC strains detected no ileX genes. Although the role of ileX in Stx2-producing EHEC strains is not clear, its function in regard to the use of rare codons and as an integration site is discussed.

Bacterial Toxins↗

A gene cluster closely related to type II secretion pathway operons of gram-negative bacteria is located on the large plasmid of enterohemorrhagic Escherichia coli O157 strains.

Analysis of 14.162 kb of DNA derived from plasmid pO157 of enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain EDL933, extending in the 5' direction of the recently described EHEC-hly operon, revealed 13 open reading frames (ORF) which showed great similarities to genes of members of the type II pathway secretion systems of Gram-negative bacteria. We named the ORFs etpC to etpO for EHEC type II secretion pathway. In addition, an IS911-like insertion element was found to separate the etp genes from the EHEC-hlyC gene. Hybridization experiments with a specific etp probe and various categories of enteric E. coli pathotypes revealed that the etp gene cluster occurred in all 30 EHEC strains of serogroup O157 (100%) tested and is distributed sporadically among other EHEC serogroups (60%). In addition, the etp genes were rarely detected in STEC isolated from bovine feces (10%). Moreover, it was found not to occur in enteropathogenic E. coli, enteroaggregative E. coli, enterotoxigenic E. coli and enteroinvasive E. coli. The results obtained with the etp probe were confirmed by a PCR approach to specifically detect an internal fragment of the etpD gene.

Amino Acid Sequence↗

Major histocompatibility complex (MHC) class I gene expression in single neurons of the central nervous system: differential regulation by interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha.

This study examined the effect of the pro-inflammatory cytokines interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on the induction of MHC class I-related genes in functionally mature brain neurons derived from cultures of dissociated rat hippocampal tissue. Patch clamp electrophysiology combined with single cell RT-PCR demonstrated that approximately 50% of the untreated neurons contained mRNA for MHC class I heavy chains, while, with few exceptions, the cells failed to transcribe beta2-microglobulin and TAP1/TAP2 gene transcripts. No constitutive expression of MHC class I protein was detectable by confocal laser microscopy on the surface of neurons. All neurons transcribed the alpha-chain of the interferon-type II receptor (binding IFN-gamma) along with the p55 receptor for TNF-alpha. Sustained exposure to IFN-gamma resulted in transcription of beta2-microglobulin and TAP1/TAP2 genes and MHC class I surface expression in a minor part of the neurons, but did not alter their electrophysiological activities as assessed by whole cell electrophysiology. Suppression of neuronal electric activity by the sodium channel blocker tetrodotoxin drastically increased to almost 100% IFN-gamma-mediated induction of MHC class I chains, of both TAP transporters, and of membrane expression of MHC class I protein. The effect of tetrodotoxin is at least partly reverted by the neurotransmitter glutamate. In contrast to IFN-gamma, treatment with TNF-alpha did neither upregulate TAP1/TAP2 nor beta2-microglobulin gene expression, but induced MHC class I heavy chain gene transcription in all neurons. Consequently, no MHC class I molecules were detectable on the membranes of TNF-alpha-treated neurons.

Gene Expression Regulation↗

Prognostic value of immunohistochemistry for p53 in primary soft-tissue sarcomas: a multivariate analysis of five antibodies.

Most changes of tumor suppressor p53 and its pathway involve a protein with prolonged half-life that permits immunohistochemical detection. The goal of this study was to compare the prognostic relevance of five different p53 antibodies in primary soft-tissue sarcomas (STS) with known p53 mutation status, using a multivariate Cox regression model (adjusted to tumor grading, staging, localization, tumor type, and therapy). A group of 198 primary STS of six types were investigated for p53 overexpression, using p53 antibodies DO-1, DO-7, Pab1801, Pab240, and CM-1. A positive marker frequency between 36.2% and 62.6% was detected. Out of 65 patients whose primary tumor reacted positively to all five antibodies, 52 (80%) died within the study period. Only the N-terminal-binding monoclonal antibodies DO-1, DO-7 and Pab1801 showed a multivariate correlation with survival (P = 0.0014, 0.0048 and 0.02). CM-1 and Pab240 had a univariate, but not a multivariate correlation, with a confounding effect of grading. The prognostic relevance for the five p53 antibodies was: DO-1 > Pab1801 > DO-7 > CM-1 > Pab240. This is the first study that investigates multivariately the prognostic relevance of p53 immunostaining in STS. If monoclonal antibodies with an epitope in the N-terminal region of the p53 protein (DO-1, Pab1801, DO-7) are applied, p53 immunohistochemistry provides an independent prognostic marker in STS.

Antibodies, Monoclonal↗

Immunohistochemical and clinical evaluation of cathepsin expression in soft tissue sarcomas.

Lysosomal proteases are known to enhance the spread of epithelial tumour cells, but little is known of the possible role of proteases in the growth of soft tissue sarcomas (STS). We investigated the expression of cathepsins D, B, S, H, L and procathepsin L in frozen sections of 34 STS from 34 patients by immunohistochemistry (IHC). Cathepsins D, B and H were relatively highly expressed in STS (77-91%). The expression rate of cathepsins S and L and of procathepsin L was lower (40-66%). Cathepsin S and L expression showed a moderate (P = 0.078 and P = 0.019) and procathepsin L a strong (P = 0.00001) correlation with the survival rate of STS patients. Cathepsin S expression is also correlated with the local recurrence rate (P < 0.01). Lysosomal proteases may play a role in STS progression, and cathepsin expression may also have significance as a prognostic factor in STS.

Adult↗

[Economic aspects of modern inhalation anesthetics with sevoflurane as an example].

The economic impact of the new German health care laws requires an awareness of cost-effectiveness when using newer drugs. The main goal in patient care, i.e., effective treatment, must be achieved by the rational use of restricted resources at a maximum degree of effectiveness. Economic aspects of the new inhalational anaesthetics such as sevoflurane are discussed in this article. The cost of inhalational anaesthetic agents accounts for up to 5% of all the running expenses of an anaesthesia department. The consumption and cost of an inhalational agent depend on fresh gas flow, vapour setting, and duration of anaesthesia. Comparing the cost for 1 MAC-h of anaesthesia, desflurane is more expensive at current market prices than sevoflurane and isoflurane. However, at low or minimal fresh gas flows, the price for one MAC-h is almost the same for these volatile anaesthetics. Total intravenous anaesthesia using propofol is even more expensive, partly due to wastage, i.e., opened ampoules with a remainder of propofol that has to be discarded after each case. When choosing an anaesthetic agent, the price of 1 ml liquid anaesthetic is an important factor. However, the overall cost-effectiveness analysis must balance the cost of the agent with its pharmacodynamic advantages such as more rapid recovery from anaesthesia. Furthermore, the indirect costs of side effects have to be taken into account. For example, nausea and vomiting lead to a prolonged stay in the recovery room after anaesthesia for outpatient surgery, which in turn incurs additional costs for antiemetic drugs and the extra time for nursing care. Therefore, a lower incidence of nausea and vomiting and a more rapid recovery from anaesthesia leading to earlier discharge from the recovery room may compensate for the higher price. Volatile agents account for up to 1% of the total intraoperative costs. In analysing the costs of 1 h of anaesthesia, other products such as plasma substitutes and blood products account for a much higher proportion than anaesthetic agents, and reductions or increases in costs pertaining to these products have a bigger impact on overall costs than do volatile anaesthetics. We conclude that volatile anaesthetics account for only a minor portion of the anaesthesia department budget and the cost of anaesthesia delivery. The higher market price of the new agents may be compensated for by the economic impact of fewer side effects and a shorter post-anaesthesia stay in the hospital. In analysing data for sevoflurane, this agent may be cost-effective, for example, for outpatient anaesthesia.

Anesthesia Department, Hospital↗

[Infiltrating intramuscular lipoma].

Intramuscular lipomas are rare, benign unencapsulated tumors. They are also called infiltrating lipomas because of their infiltrative growth pattern which, deeply localized, seizes the skeleton muscle. The only obvious symptom is a palpable mass. Microscopically, monovacular fat tissue shows up between the muscle fiber. In extreme cases the preexisting muscle can be totally replaced by fat tissue. A precise pathohistological examination is needed to avoid the mistaken diagnosis of a well-differentiated liposarcoma. Late diagnosis, the extent and the localization of the tumor often do not allow for an R0 resection and influence the postoperative recurrence rates, which lie between 3 and 62%. R0 resections are not desirable when postoperative severe loss of function can be expected. Malfunctions will slowly take place and can greatly be compensated, in contrast to a radical procedure with immediate loss of function.

Aged↗

[Treatment of patients with thromboses of the basilar artery and locked-in syndrome. An ethical dilemma].

Decisions regarding the extent of treatment of severely ill patients can be an ethical dilemma when life-prolonging intensive care contradicts the goal of avoiding unnecessary suffering on the part of the patient. Here we present the results of a written survey of physicians on neurological intensive care units in Germany regarding the treatment of patients with basilar artery thrombosis and locked-in syndrome. 52% of the 93 physicians who replied advocated not treating severe infections with antibiotics, 38% were in favor of stopping intensive care. In contrast, 55% recommended intubating the patient in the presence of swallowing disturbances and imminent aspiration. 58% were in favor of discussing these problems in detail with the patient, and 87% advocated discussing them with relatives. Nearly all physicians (97%) recommended using adequate amounts of opiates and benzodiazepines. In very rare cases, 99% would agree to the use of passive euthanasia and 19% to active euthanasia. These findings illustrate the current disagreement on some of the important treatment decisions among physicians on neurological intensive care units. An open exchange of views on these questions could facilitate the appropriate consideration of ethical matters in the treatment of these patients.

Adult↗

[Necrotizing enterocolitis (NEC)].

Necrotizing enterocolitis is a serious abdominal disease in infants during the first 2 months of life. The earliest radiographic finding on frontal abdominal films is initially distension of the small bowel, secondly of the colon, and pneumatosis intestinalis. Pneumatosis intestinalis is not pathognomonic for necrotizing enterocolitis; it can occur throughout life in different abdominal diseases. It can be a serious prognostic sign for abdominal ileus, but it may also occur in non-critically ill patients. Radiographic diagnosis in childhood is achieved with a frontal film of the abdomen in the prone position, and to detect a possible perforation, a left lateral abdominal decubitus exposure is necessary. Sonography and duplex sonography are helpful in evaluating progressive changes, the clinical course and the differential diagnosis.

Diagnosis, Differential↗