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Biomedical subjects

Peter Ott

Publications and source records attributed to Peter Ott.

At least 19 recordsLinked to original sources
PubMed2006

[Surgical risk for patients with liver disease].

Liver disease increases surgical risk. Thus, in patients with cirrhosis, the mortality after abdominal or heart surgery is 50-75% in Child-Pugh C, 20-30% in B and near normal in Child-Pugh A. Stable autoimmune hepatobiliary disease and steatosis without inflammation do not increase surgical risk, but the mortality after major abdominal surgery is increased in patients with fulminant hepatic failure (>90%), alcoholic hepatitis (50%) and acute viral hepatitis (10-15%).

Elective Surgical Procedures↗
PubMed2006

[Hepatic pruritus].

Pruritus is a key symptom of hepatic disease. In severe cases, this symptom ruins the patient's quality of life. Most likely it is caused by a protein-bound bile acid (metabolite) that stimulates opioid receptors in the brain. Symptomatic treatments that can reduce pruritus in selected patients include opioid receptor antagonists, biliary diversion, cholestyramine, ursodeoxycholic acid, rifampicin and phenobarbitone. Plasmapheresis or albumin dialysis may be useful when other treatment fails.

Adult↗
PubMed2006

Brain metabolism of 13N-ammonia during acute hepatic encephalopathy in cirrhosis measured by positron emission tomography.

Animal studies and results from 13N-ammonia positron emission tomography (PET) in patients with cirrhosis and minimal hepatic encephalopathy suggest that a disturbed brain ammonia metabolism plays a pivotal role in the pathogenesis of hepatic encephalopathy (HE). We studied brain ammonia kinetics in 8 patients with cirrhosis with an acute episode of clinically overt HE (I-IV), 7 patients with cirrhosis without HE, and 5 healthy subjects, using contemporary dynamic 13N-ammonia PET. Time courses were obtained of 13N-concentrations in cerebral cortex, basal ganglia, and cerebellum (PET-scans) as well as arterial 13N-ammonia, 13N-urea, and 13N-glutamine concentrations (blood samples) after 13N-ammonia injection. Regional 13N-ammonia kinetics was calculated by non-linear fitting of a physiological model of brain ammonia metabolism to the data. Mean permeability-surface area product of 13N-ammonia transfer across blood-brain barrier in cortex, PS(BBB), was 0.21 mL blood/min/mL tissue in patients with HE, 0.31 in patients without HE, and 0.34 in healthy controls; similar differences were seen in basal ganglia and cerebellum. Metabolic trapping of blood 13N-ammonia in the brain showed neither regional, nor patient group differences. Mean net metabolic flux of ammonia from blood into intracellular glutamine in the cortex was 13.4 micromol/min/L tissue in patients with cirrhosis with HE, 7.4 in patients without HE, and 2.6 in healthy controls, significantly correlated to blood ammonia. In conclusion, increased cerebral trapping of ammonia in patients with cirrhosis with acute HE was primarily attributable to increased blood ammonia and to a minor extent to changed ammonia kinetics in the brain.

Acute Disease↗
PubMed2006

Electrocardiographic markers of sudden death.

The 12-lead ECG has limited utility to predict the risk for sudden cardiac death in common cardiac diseases such as coronary artery disease and idiopathic dilated cardiomyopathy. However, it is quite useful in diagnosing less common cardiac conditions that are associated with an increased risk for sudden death.

Biomarkers↗
PubMed2005

Homozygosity for a gross partial gene deletion of the C-terminal end of ATP7B in a Wilson patient with hepatic and no neurological manifestations.

We identified a partial gene deletion of ATP7B in a patient with Wilson disease with hepatic onset. The deletion covered exon 20 including major parts of the flanking introns. The breakpoints were identified and the size of the deletion determined to be 2144 bp. The deletion is predicted to lead to a mutated protein product containing 45 aberrant amino acids after transmembrane domain 7, and lacking the transmembrane domain 8 as well as the entire C-terminal cytoplasmic tail. This is the first time a partial gene deletion has been demonstrated in ATP7B. The patient presented at age 10 with hepatic manifestations, including severe jaundice, hepato-splenomegaly, ascites, and spider naevi. The liver biopsy showed fibrosis and early signs of cirrhosis. There was a Kayser-Fleischer ring but no neurological manifestations. All symptoms disappeared with penicillamine therapy. This suggests that the C-terminal cytoplasmatic tail of ATP7B, is not essential for its neurological function. Large deletions in ATP7B may be an overlooked cause of Wilson disease. Patients that are homozygotes for deletions may be valuable for the understanding of the function of various regions of the ATP7B protein.

Adenosine Triphosphatases↗
PubMed2005

Maintained cerebral and skeletal muscle oxygenation during maximal exercise in patients with liver cirrhosis.

BACKGROUND/AIMS: In cirrhotic patients, insufficient redistribution of blood from splanchnic organs to the central circulation could limit blood supply to skeletal muscles and the brain during exercise. METHODS: Eight cirrhotic patients performed incremental cycling to exhaustion (74 (49-123) W; median with range). RESULTS: Heart rate increased from 68 (62-88)beats/min at rest to 142 (116-163)beats/min, cardiac output from 5.1 (3.3-7.2) to 12.9 (8.5-15.9)l/min, and mean arterial pressure from 89 (75-104) to 115 (92-129)mmHg (P<0.05), while the indocyanine green elimination determined hepatosplanchnic blood flow declined from 0.97 (0.55-1.46) to 0.62 (0.36-1.06)l/min (P<0.05). As assessed by near-infrared spectrophotometry, cerebral oxygenation (NIRS) was 61% (48-85%) and increased to 72% (57-86%) during exercise (P<0.05). The NIRS determined oxygenation of the vastus lateralis muscle also increased: the concentrations of oxygenated haemoglobin by 5.9 (0.57-9.47)micromol/l, deoxygenated haemoglobin by 7.2 (1.8-12.0)micromol/l, and thus total haemoglobin by 12.1 (3.6-21.5)micromol/l (P<0.05). CONCLUSIONS: In patients with cirrhosis, exercise reduces hepatosplanchnic blood flow, while O(2) supply to muscle and brain appears to increase indicating that blood redistribution from splanchnic organs does not limit blood flow to working muscles and the brain.

Adult↗
PubMed2005

Cerebral metabolic disturbances in the brain during acute liver failure: from hyperammonemia to energy failure and proteolysis.

Several observations suggest that patients with fulminant hepatic failure may suffer from disturbances in cerebral metabolism that can be related to elevated levels of arterial ammonia. One effect of ammonia is the inhibition of the rate limiting TCA cycle enzyme alpha-ketoglutarate dehydrogenase (alphaKGDH) and possibly also pyruvate dehydrogenase, but this has been regarded to be of no quantitative importance. However, recent studies justify a revision of this point of view. Based on published data, the following sequence of events is proposed. Inhibition of alphaKGDH both enhances the detoxification of ammonia by formation of glutamine from alpha-ketoglutarate and reduces the rate of NADH and oxidative ATP production in astrocytic mitochondria. In the astrocytic cytosol this will lead to formation of lactate even in the presence of sufficient oxygen supply. Since the aspartate-malate shuttle is compromised, there is a risk of depletion of mitochondrial NADH and ATP unless compensatory mechanisms are recruited. One likely compensatory mechanism is the use of amino acids for energy production. Branched chain amino acids, like isoleucine and valine can supply carbon skeletons that bypass the alphaKGDH inhibition and maintain TCA cycle activity. Large-scale consumption of certain amino acids can only be maintained by cerebral proteolysis, as has been observed in these patients. This hypothesis provides a link between hyperammonemia, ammonia detoxification by glutamine production, cerebral lactate production, and cerebral catabolic proteolysis in patients with FHF.

Ammonia↗
PubMed2005

Elevated temperature during reproductive development affects cone traits and progeny performance in Picea glauca x engelmannii complex.

Two temperature regimes were applied during reproductive development of seed and pollen cones of interior spruce (Picea glauca (Moench) Voss and Picea engelmannii (Parry) complex) to determine temperature effects on the adaptive traits of progeny. In Experiment 1, identical crosses were made on potted interior spruce using untreated pollen followed by exposure to a day/night temperature of 22/8 or 14/8 degrees C with a 12-h photoperiod during the stages of reproductive development from post-pollination to early embryo development. Frost hardiness and growth of progeny from seed produced in the two temperature treatments were measured over a 4-year period. Elevated temperature significantly affected both seed-cone development and the adaptive properties of the progeny. Seed cones exposed to the 22/8 degrees C treatment reached the early embryo stage in 53 days versus 92 days in the 14/8 degrees C treatment. Seed yields, cotyledon emergence and percent germination were also significantly enhanced by the 22/8 degrees C treatment. Progeny from seed produced in the higher temperature treatment showed significantly reduced spring and fall frost hardiness, but the elevated temperature treatment had no significant effects on time of bud burst, growth patterns or final heights. In Experiment 2, single ramets of the same clone were subjected to a day/night temperature of 20/8 or 10/8 degrees C during pollen cone development, starting from meiosis and ending at pollen shedding. The two populations of pollen were then crossed with untreated seed cones. Compared with pollen cones exposed to the 10/8 degrees C treatment, pollen cones exposed to the 20/8 degrees C treatment during development reached the shedding stage 2-4 weeks earlier, whereas pollen yields, in vitro viability and fertility (seed set) were significantly lower; however, the resulting progeny displayed no treatment differences in frost hardiness or growth after 1 year. Results suggest that seed orchard after-effects could be caused by temperature differences between orchard site and parent tree origin and that this effect acts on maternal development. Gametophytic (pollen or megagametophyte or both) and early embryo (sporophytic) selection are possible mechanisms that may explain the observed results. Although the effects are biologically significant, they are relatively small and do not justify changes in current deployment strategies for seed orchard seed.

Hot Temperature↗
PubMed2005

Imaging with tilted surfaces: an efficient matrix method for the generalized Scheimpflug condition and its application to rotationally symmetric triangulation.

An efficient two-dimensional matrix method is presented that facilitates the design of optical systems with tilted surfaces for which the requirement or knowledge of the orientation of the image plane is necessary, i.e., for which a generalized Scheimpflug condition is needed. In more general terms, the method results in imaging properties of second-order expansion, but the method is linear. Therefore the complexity of the design process is considerably reduced. The strength of the design method is demonstrated in detail for a novel application in which a reflective optical system of several surfaces is required for rotationally symmetric triangulation.

Journal Article↗
PubMed2004

The CSF and arterial to internal jugular venous hormonal differences during exercise in humans.

Strenuous exercise increases the cerebral uptake of carbohydrate out of proportion to that of oxygen, but it is unknown whether such enhanced carbohydrate uptake is influenced by the marked endocrine response to exercise. During exhaustive exercise this study evaluated the a-v differences across the brain (a-v diff) of hormones that could influence its carbohydrate uptake (n= 9). In addition, neuroendocrine activity and a potential uptake of hormones via the cerebrospinal fluid (CSF) were assessed by lumbar puncture postexercise and at rest (n= 6). Exercise increased the arterial concentration of noradrenaline and adrenaline, but there was no cerebral uptake. However, following exercise CSF noradrenaline was 1.4 (0.73-5.5) nmol l(-1), and higher than at rest, 0.3 (0.19-1.84) nmol l(-1) (P < 0.05), whereas adrenaline could not be detected. Exercise increased both the arterial concentration of NH(4)(+) and its a-v diff, which increased from 1 (-12 to 5) to 17 (5-41) micromol l(-1) (P < 0.05), while the CSF NH(4)(+) was reduced to 7 (0-10) versus 11 (7-16) micromol l(-1) (P < 0.05). There was no release from, or accumulation in the brain of interleukin (IL)-6, tumour necrosis factor (TNF-alpha), heatshock protein (HSP72), insulin, or insulin-like growth factor (IGF)-I. The findings indicate that for maximal exercise, the concentration of noradrenaline is increased within the brain, whereas blood borne hormones and cytokines are seemingly unimportant. The results support the notion that the exercise-induced changes in brain metabolism are controlled by factors intrinsic to the brain.

Adult↗