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Biomedical subjects

J Linderman

Publications and source records attributed to J Linderman.

5 recordsLinked to original sources

Genotyping of Helicobacter pylori strains in formalin-fixed or Formaldehyde-sublimate-fixed paraffin-embedded gastric biopsy specimens.

Different genotypes of Helicobacter pylori can play a role in the development of atrophic gastritis, peptic ulcer disease, and gastric carcinomas. In this study the authors developed polymerase chain reaction assays for the detection and identification of vacA (s- and m-regions), cagA, and iceA genotypes of H. pylori in formalin-fixed or formaldehyde-sublimate-fixed paraffin-embedded gastric biopsy specimens. Polymerase chain reaction products were analyzed by reverse hybridization on a line-probe assay. Complete genotyping was achieved in 26 of 28 samples (93%), and multiple genotypes, indicating the presence of multiple strains, were detected in nine samples (32%). This genotyping method offers the possibility for long-term retrospective studies on H. pylori genotypes and gastric pathology in the same archival gastric tissue specimens.

Bacterial Proteins↗

The effects of sodium bicarbonate and pyridoxine-alpha-ketoglutarate on short-term maximal exercise capacity.

The purpose of this study was to determine the effects of the simultaneous use of pyridoxine-alpha-ketoglutarate (PAK) and sodium bicarbonate (NaHCO3) on short-term maximal exercise capacity in eight well-trained male cyclists. The study consisted of the determination of maximal power output and the administration of various combinations of placebos, PAK and NaHCO3, followed by a short-term maximal exercise test. To determine maximal power output (power(max)), the subjects performed a continuous, incremental test on a Monark bicycle ergometer to symptom limited maximum (test 1). To determine the effects of NaHCO3 and PAK on short-term maximal exercise performance, the subjects were administered either placebo (PLA), PAK and sodium bicarbonate (P/B), PAK and placebo (PAK), or sodium bicarbonate and placebo (BIC) prior to performing short-term maximal exercise (test 2). Oral tablets of NaHCO3 and PAK were given in doses of 200 mg kg-1 and 50 mg kg-1 respectively. The subjects pedalled at the power output corresponding to 100% of their VO2 max at 70 rev min-1 until voluntary cessation or until they were unable to maintain pedal revolution rate. Venous blood samples were drawn at rest (RES), cessation of exercise (CES) and after 2 min of recovery (REC) and analysed for lactate, pH and bicarbonate ion concentration. The subjects attained an average maximum power output of 377 +/- 20 W during the graded maximal pre-test (test 1). There were no significant differences between treatments in the ability to sustain power(max) during test 2. During test 2, the subjects were able to sustain power(max) for 7.6 +/- 4.3 min with P/B, 6.7 +/- 2.9 min with PAK, 7.3 +/- 4.9 min with BIC and 6.9 +/- 2.7 min with placebo (mean +/- S.E.). Blood lactate (BLa) was significantly elevated at cessation of exercise and remained elevated during recovery, but there were no significant differences between treatments. Bicarbonate fell significantly during exercise and recovery in each treatment. At rest, bicarbonate levels were significantly higher in both the P/B and BIC than in the PAK or PLA treatments. Pooled data from the P/B and BIC treatments demonstrated a significant increase in pH at rest and end of exercise when compared to PLA treatment. These data suggest that sodium bicarbonate rather than PAK was responsible for this increase. In summary, our data suggest that in the dosages used in this study, administration of sodium bicarbonate or PAK, alone or in combination, is ineffective in increasing short-term maximal exercise capacity.

Adult↗

A comparison of blood gases and acid-base measurements in arterial, arterialized venous, and venous blood during short-term maximal exercise.

The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test II). During test II arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO3-), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P less than 0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r = 0.83 [regression equation: BEa = (0.84 BEav)-0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3 mmol.l-1) and higher than both venous and arterialized venous La at EE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Analysis of mammalian cell growth factor receptor dynamics.

We have proposed a mathematical model for the events following binding of EGF to cell surface receptors with the aim of elucidating possible mechanisms associated with a lack of responsiveness to EGF mitogenic stimulation. Comparison of our model calculations with the experiments of Schaudies et al. suggests at least two possible mechanisms: an increase in the rate of receptor synthesis, or an increase in the fraction of internalized receptors that are recycled to the cell surface. Discrimination between these alternatives requires experimental measurement of cell receptor quantities, such as the number of surface complexes or the amount of degraded receptor. At the present time, we speculate that an increase in the fraction of receptors recycled seems to be the more likely explanation.

Animals↗