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Biomedical subjects

P Kölle

Publications and source records attributed to P Kölle.

10 recordsLinked to original sources
PubMed2004

Increased intestinal permeability in patients with inflammatory bowel disease.

Intestinal permeability can be measured by the sugar absorption test. This test is based on determining the ratio of the urinary excretion of a large and a small carbohydrate after oral administration. The aim of this study was to determine which combination of carbohydrates used in the test gives the highest correlation with disease activity in inflammatory bowel disease. 26 patients with Crohn's disease, 21 patients with ulcerative colitis and 27 healthy control subjects were included in the study. The patients with inflammatory bowel disease had either minimal or highly active disease or were in remission. Two disaccharides (lactulose: L, and cellobiose: C) and two smaller carbohydrates (rhamnose:R, and mannitol:M) were given orally and the urinary excretion was measured by high pressure liquid chromatography followed by pulsed amperometric electrochemical detection on a gold electrode. The ratios C/R, L/R, C/M and L/M were used as indicators for intestinal permeability. - There were no side effects of oral sugar administration. All patients tolerated the test well. Lactulose, rhamnose and cellobiose concentrations are easily be measured in the urine whereas mannitol measurement requires the use of an anion exchanger. This produced inconsistent results. Patients with Crohn's disease or with ulcerative colitis had increased permeability indices in comparison to healthy controls, even in remission. The L/R ratio gave a better differentiation between the healthy controls and patients with active disease than the other agents. Changes in disease activity are best reflected by use of cellobiose/rhamnose excretion quotient.

Adolescent↗
PubMed2002

A G468-T AMPD1 mutant allele contributes to the high incidence of myoadenylate deaminase deficiency in the Caucasian population.

Myoadenylate deaminase deficiency is the most common metabolic disorder of skeletal muscle in the Caucasian population, affecting approximately 2% of all individuals. Although most deficient subjects are asymptomatic, some suffer from exercise-induced myalgia suggesting a causal relationship between a lack of enzyme activity and muscle function. In addition, carriers of this derangement in purine nucleotide catabolism may have an adaptive advantage related to clinical outcome in heart disease. The molecular basis of myoadenylate deaminase deficiency in Caucasians has been attributed to a single mutant allele characterized by double C to T transitions at nucleotides +34 and +143 in mRNA encoded by the AMPD1 gene. Polymerase chain reaction-based strategies have been developed to specifically identify this common mutant allele and are considered highly sensitive. Consequently, some laboratories preferentially use this technique over other available diagnostic tests for myoadenylate deaminase deficiency. We previously identified a G468-T mutation in one symptomatic patient who was only heterozygous for the common AMPD1 mutant allele. In this report, nine additional individuals with this compound heterozygous genotype are revealed in a survey of 48 patients with documented deficiency of skeletal muscle adenosine monophosphate deaminase and exercise-induced myalgia. Western blot analysis of leftover biopsy material from one of these individuals does not detect any immunoreactive myoadenylate deaminase polypeptide. Baculoviral expression of the G468-T mutant allele produces a Q156H substitution enzyme exhibiting labile catalytic activity. These combined results demonstrate that the G468-T transversion is dysfunctional and further indicate that AMPD1 alleles harboring this mutation contribute to the high incidence of partial and complete myoadenylate deaminase deficiency in the Caucasian population. Consequently, genetic tests for abnormal AMPD1 expression designed to diagnose patients with metabolic myopathy, and to evaluate genetic markers for clinical outcome in heart disease should not be based solely on the detection of a single mutant allele.

AMP Deaminase↗
PubMed2001

[Mistakes in general husbandry of ornamental fish].

Mistakes in general husbandry conditions of ornamental fish can consist in insufficient quality of water, inadequate feeding, equipment and social structure and poor prophylactic measures. Clinical symptoms are generally not specific.

Animal Husbandry↗
PubMed1998

[Keeping reptiles].

Keeping of reptiles in captivity is permanently increasing. As there exists such a great number of species of reptiles, the conditions of the natural habitat of the kept species have to be imitated as exactly as possible. Disorders in reptiles are often caused by inadequate maintainance.

Animal Diseases↗
PubMed1997

[Pain in the breeding of fish].

Excessive breeding leading to suffering in animals only exists in ornamental fish, especially in gold fish or poecillids. These varieties are physically handicapped in locomotion, feeding and/or reproduction in comparisation to wild fish.

Animals↗
PubMed1996

[Blood parameters as an aid in the diagnosis of reptile diseases].

As ill reptiles only show nonspecific clinical signs, blood chemistry parameters are a valuable help in diagnosis. Practicable sites for obtaining blood of snakes, sauria and chelonians are vena coccygealis ventralis and cardiac puncture, of chelonians also vena jugularis, axillaris and coccygealis dorsalis. The following blood parameters were investigated: number of erythrocytes and leucocytes, urea, uric acid, creatinine, AST (GOT), ALT (GPT) GLDH, AP, total bilirubin, CK, LDH, lipase, alpha-amylase, calcium, phosphorus, sodium, potassium, chloride and total protein. Especially for diagnosing nephropathies evaluation of urea and uric acid proved to be valuable.

Animal Diseases↗
PubMed1995

Capillary electrophoresis for screening of adenylosuccinate lyase deficiency.

We report a new screening method for adenylosuccinate lyase (ASase) deficiency using capillary electrophoresis (CE). This enzyme defect causes secondary autism and psychomotor retardation in early childhood. In all body fluids of these patients, two succinylpurine metabolites can be found that are normally not detectable: succinyladenosine and succinylaminoimidazole carboxamide (SAICA) riboside. A Beckman P/ACE 2050 capillary electrophoresis system was used with a 47.1 cm capillary, 75 microns ID, and the P/ACE Beckman UV absorbance detector. Untreated urine, injected for 1 s, was separated in a pH 8.63 borate buffer at 20 kV. The two succinylpurines (migration times 13.36 and 13.60 min) were detected at 254 nm only in urine of patients with ASase deficiency but not in control samples.

Adenosine↗