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S Klemm

Publications and source records attributed to S Klemm.

13 recordsLinked to original sources

[31P-MR spectroscopy of the brain in patients with anorexia nervosa: characteristic differences in the spectra between patients and healthy control subjects].

PURPOSE: To investigate whether 31 P-MR spectroscopy can detect reduced concentrations of high-energy phosphates, like PCr and NTP, caused by decreased metabolic activity in the brain of patients with anorexia nervosa (AN) and, furthermore, whether any impairment of the cerebral membrane metabolism can be derived from the spectra. MATERIAL AND METHODS: 10 female patients, age range 12 - 20 years and mean BMI (body mass index) of 14.8 +/- 1.6 kg/m 2, with clinically diagnosed AN (ICD-10, F50.0) and 10 healthy control subjects, age range 12 - 21 years and mean BMI 19.0 +/- 2.1 kg/m 2, without nutritional disturbances: were investigated. 31P-MR spectroscopy was performed with a 1.5 T MRI unit using single volume selection in the frontal/prefrontal region of brain. Relative metabolic concentrations were quantified by normalizing the peak areas of the metabolites with the total area of the complete phosphorous spectrum, P tot, as well as with the peak area of beta-NTP. RESULTS: Significant differences between the two groups were observed for the metabolic ratios PDE/P tot, PDE/beta-NTP and alpha-NTP/P tot which were lower in the patient group except for alpha-NTP/P tot. These ratios also revealed a statistically significant correlation with the BMI (r PDE/Ptot = 0.747, r PDE/beta-NTP = 0.57, r alpha-NTP/Ptot = -0.56; p </= 0.1). Reduced relative concentrations of PCr/P tot, beta-NTP/P tot or Pi/P tot were not encountered. CONCLUSION: The lowered PDE/P tot ratio for patients with AN and its correlation with BMI suggests that decreased BMI induces compositional changes of the phospholipids in the brain, which decrease the fraction of mobile phospholipids.

Adolescent↗

31P-MR spectroscopy in children and adolescents with a familial risk of schizophrenia.

Based on a previous report [9] on alterations of membrane phosphorus metabolism in asymptomatic family members of schizophrenic patients, the aim of the present study was to extend and improve the evaluation and data processing of (31)P spectroscopic data obtained from a larger study population by including an analysis of the broad spectral component (BC) of membrane phospholipids (PL). Eighteen children and siblings of patients with schizophrenia and a gender- and age-matched control group of 18 healthy subjects without familial schizophrenia were investigated with phosphorus magnetic resonance spectroscopy ((31)P-MRS) by using image selected in vivo spectroscopy (ISIS) in the dorsolateral prefrontal regions (DLPFR) of the brain. Spectral analysis was performed by using both the full and truncated FID to estimate metabolic peak ratios of different (31)P metabolites and the intensity and linewidth of the broad component. A significantly higher PDE level (p<0.01) and increased linewidth of the PDE components were observed for the high-risk group compared with the control group (p=0.02). No significant differences were observed for PME as well as for other (31)P-metabolites. No differences were observed between the left and right hemispheres for different normalised (31)P-metabolic levels. Decreased intensities (p=0.03) and smaller linewidths (p=0.01) were obtained for the broad component in the high-risk group. Impairments of membrane metabolism that are typical for schizophrenic patients are partially observed in adolescent asymptomatic family members of schizophrenics, including increased levels of low molecular PDE compounds indicating increased membrane degradation processes, no changes for PME, and decreased intensities and linewidths of the BC indicating changes in the composition and fluidity of membrane phospholipids. Despite limitations to completely suppress fast-relaxing components by dismissing initial FID data points, the spectroscopic results indicate additional changes in the membrane metabolism of high-risk subjects beyond changes of synthesis and degradation.

Adolescent↗

[Risk for schizophrenia and diagnostic image of cerebral membrane metabolism].

In recent years neurobiological research on the etiology of schizophrenia has became increasingly important. In terms of a vulnerability-stress model, structural and functional cerebral alterations in schizophrenics and subjects with a genetic risk for schizophrenia are presented together with hypotheses for disturbances of neurodevelopment or neurodegeneration developed from these implications. A detailed description follows of a neurobiochemical paradigm on the disturbance of metabolism of membrane-phospholipids. 31Phosphorous Magnetic Resonance Spectroscopy allows the detection of indicators of this possible endo-phenotype. The possibilities and limitations of this method are explained, as are findings up to the present. Finally, it is discussed that specific pre-, peri- and postnatal influences on the cerebral metabolism of lipids, and thus on cerebral development, may be related to structural and functional cerebral changes in schizophrenia.

Biomarkers↗

Cerebral phosphate metabolism in first-degree relatives of patients with schizophrenia.

OBJECTIVE: Most phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS) studies have described measures of lower membrane anabolism or greater catabolism in the frontal lobes of patients with schizophrenia. The purpose of the present study was to evaluate whether these findings can also be detected in young subjects at genetic risk for schizophrenia. METHOD: Fourteen children and siblings of patients with schizophrenia (mean age=16.7 years) and 14 comparison subjects (mean age=16.9 years) were included in a (31)P-MRS study of the frontal lobe. RESULTS: The high-risk subjects had significantly lower mean ratios of phosphomonoesters to phosphodiesters (0.25 versus 0.31) and higher mean phosphodiester values (37.59% versus 34.87%) than comparison subjects. CONCLUSIONS: These findings suggest greater phospholipid breakdown even in young first-degree relatives of patients with schizophrenia. This suggestion is discussed with respect to the membrane phospholipid hypothesis of schizophrenia.

Adolescent↗

Effect of intraoperative angiotensin-converting enzyme inhibition by quinaprilat on hypertension after coronary artery surgery.

Activation of the renin-angiotensin system during cardiopulmonary bypass (CPB) may be involved in early postoperative hypertension after coronary artery bypass grafting (CABG). As hypertensive episodes may be deleterious in the immediate postoperative period, we have assessed the effects of prophylactic treatment with the angiotensin-converting enzyme inhibitor quinaprilat in an open study. During steady state CPB, patients received quinaprilat 0.02 mg kg-1 (group A, n = 10), quinaprilat 0.04 mg kg-1 (group B, n = 10) or saline solution (group C, n = 10) as an i.v. bolus dose. Sodium nitroprusside (SNP) was given after operation when systolic arterial pressure was > 150 mm Hg. Requirements for SNP 1 h after arrival in the ICU were significantly less in groups A (two of 10) and B (two of 10) than in group C (eight of 10). Also, patients in group C had a greater systolic arterial pressure compared with groups A and B. There were no significant differences between groups in diastolic arterial pressure, heart rate, cardiac index or cardiac filling pressures. We conclude that quinaprilat can be used during CABG to reduce the incidence of postoperative hypertension. Further studies of the efficacy and safety of this technique are necessary.

Angiotensin-Converting Enzyme Inhibitors↗

Allelic losses on chromosome band 11q13 in aldosterone-producing adrenal tumors.

We examined loss of heterozygosity (LOH) in 14 aldosterone-producing adrenal tumors, with six linearly ordered restriction fragment length polymorphism (RFLP) markers that map within a 12-cM region containing the MEN1 locus on 11q13. Among 11 tumors that were informative for at least one marker, five showed LOH at one or more loci, and two distinct regions of deletion were identified. The proximal region overlapped with the location of the MEN1 locus previously predicted by linkage analyses in MEN1 families and the commonly deleted region in hyperparathyroid tumors. This suggests that one of the genes associated with development of aldosterone-producing adrenal tumors may coincide with the MEN1 locus, and that a second gene, distal to the MEN1 locus, may also play a role in the development of this type of tumor.

Adrenal Gland Neoplasms↗

Detection of renin mRNA in aldosterone-producing adenomas by polymerase chain reaction.

1. Ribonucleic acid (RNA) was extracted from two normal human adrenal cortices and from five aldosterone-producing adenomas (APA). 2. The five APA could be categorized, on the basis of in vivo aldosterone responsiveness to angiotensin infusion and upright posture, into two APA responsive to both stimuli, two responsive only to angiotensin infusion, and one unresponsive to either stimulus. 3. RNA was reverse transcribed and coamplified by polymerase chain reaction (PCR) with an internal standard of renin complementary DNA (cDNA) containing a 60 base pair insertion. Renin mRNA in the APA was compared with normal adrenals. 4. Renin mRNA was greater than normal in the two APA responsive to both stimuli and less than, or similar to normal, in the two APA responsive only to angiotensin infusion. Renin mRNA was also less than, or similar to normal, in the APA unresponsive to either stimulus. 5. These findings support a possible role for adrenal renin in the development and biochemical behaviour of angiotensin-responsive APA.

Adenoma↗