Fetal heart rate variability reveals differential dynamics in the intrauterine development of the sympathetic and parasympathetic branches of the autonomic nervous system.

The aim of this study was to investigate the hypothesis that fetal beat-to-beat heart rate variability (fHRV) displays the different time scales of sympatho-vagal development prior to and after 32 weeks of gestation (wks GA). Ninety-two magnetocardiograms of singletons with normal courses of pregnancy between 24 + 1 and 41 + 6 wks GA were studied. Heart rate patterns were either quiet/non-accelerative (fHRP I) or active/accelerative (fHRP II) and recording quality sufficient for fHRV. The sample was divided into the GA groups <32 wks GA/>32 wks GA. Linear parameters of fHRV were calculated: mean heart rate (mHR), SDNN and RMSSD of normal-to-normal interbeat intervals, power in the low (0.04-0.15 Hz) and high frequency range (0.15-0.4 Hz) and the ratios SDNN/RMSSD and LF/HF as markers for sympatho-vagal balance. fHRP I is characterized by decreasing SDNN/RMSSD, LF/HF and mHR. The decrease is more pronounced <32 wks GA. Beyond that GA SDNN/RMSSD is predominantly determined by RMSSD during fHRP I and by SDNN during fHRP II. In contrast to fHRP I, during fHRP II, mHR is positively correlated to SDNN/RMSSD instead of SDNN >32 wks GA. LF/HF increases in fHRP II during the first half of the third trimester. Non-accelerative fHRP are indicative of parasympathetic dominance >32 wks GA. In contrast, the sympathetic accentuation during accelerative fHRP is displayed in the interrelations between mHR, SDNN and SDNN/RMSSD. Prior to 32 wks GA, fHRV reveals the increasing activity of the respective branches of the autonomic nervous system differentiating the types of fHRP.

Patterns of cerebrospinal fluid pathology correlate with disease progression in multiple sclerosis.

Multiple sclerosis is a chronic inflammatory and demyelinating disease of the CNS with, as yet, an unknown aetiology. Temporal profile, intensity and treatment responses are highly variable in multiple sclerosis suggesting pathogenetic heterogeneity. This hypothesis has been supported by histopathological studies disclosing at least four different subtypes of acute demyelinating lesions. Although stratification of multiple sclerosis patients into these categories would be extremely helpful for clinical studies, this approach is impractical as it requires brain biopsy. In this study we investigated CSF cytology from 60 multiple sclerosis patients by flow cytometry. We identified different patterns of CSF cytology, which were independent of immunological parameters in the peripheral blood. The most variable CSF parameter was the B cell to monocyte ratio, which remained stable during different phases of disease in selected patients. The ratio correlated with disease progression but not with disability or disease duration in a retrospective, consecutive analysis. A high ratio (predominance of B cells) was associated with more rapid disease progression, whereas a low ratio (predominance of monocytes) was found in patients with slower progression. Our study demonstrates the existence and potential clinical relevance of different CSF cytology patterns. We hypothesize that CSF cytology patterns may reflect the heterogeneity in the pathogenesis of multiple sclerosis.

Fecal bile acid excretion pattern in cholecystectomized patients.

The fecal bile acid excretion pattern was investigated in 25 cholecystectomized and 26 noncholecystectomized patients as a measure for the exposure of the colonic mucosa to bile acids. Separation of free, conjugated, and sulfated bile acids was achieved by liquid-gel chromatography using DEAP Sephadex LH-20 and quantification of individual bile acids by gas-liquid chromatography. Total bile acid concentration was higher in cholecystectomized (5.33 +/- 0.71 mg/g) than in noncholecystectomized patients (3.69 +/- 0.65 mg/g). Deoxycholic acid excretion was elevated in cholecystectomized patients in three aspects: the concentration of deoxycholic acid was higher (2.92 +/- 0.39 mg/g and 1.71 +/- 0.35 mg/g, respectively), its percentage proportion of total bile acids was increased (53.9 +/- 2.8% and 41.4 +/- 3.1%, respectively), and its daily output was twice as large as that in patients without previous cholecystectomy (63.2 +/- 11.5 and 32.9 +/- 5.9 mg/day, respectively).

Fecal bile acids in patients with adenomatous polyps of the colon. Case-control study.

Populations with a high colonic cancer incidence excrete larger amounts of bile acids in their feces. Patients with adenomatous polyps of the colon are at a greater risk of developing colonic cancer. Therefore, we studied the fecal bile acid excretion pattern in 12 patients with adenomatous polyps in comparison to 12 control subjects matched for age and sex. Analysis of bile acids was performed using liquid-gel chromatography for the separation of free, conjugated and sulfated bile acids and gas liquid chromatography for quantitation. This case-control study did not confirm the previous finding of an increased fecal bile acid excretion in patients with adenomatous polyps. Total bile acid excretion, the pattern of the primary and major secondary bile acids and their mode of conjugation were essentially the same for both groups. This negative result may be explained by similar dietary habits of both groups.

Fecal bile acid excretion pattern in colonic cancer patients.

Epidemiological investigations have shown an association between the incidence of colonic cancer, dietary habits, and bile acid metabolism. We analyzed the fecal bile acid excretion pattern in 23 patients with colonic carcinoma and in 21 controls. We determined the total bile acid concentration, the concentration of individual bile acids as a measure for bacterial degradation, and the degree of sulfation. Separation of nonsulfated and sulfated bile acids was achieved by the lipophilic anion-exchanger DEAP-Sephadex-LH 20, quantification of individual bile acids by gas-liquid chromatography. Corresponding with a significantly lower stool mass per day, colonic cancer patients had a lower daily bile acid excretion. But we found no statistically significant difference between the groups in the fecal concentration of total or individual bile acids or their mode of conjugation. There was a wide variation of total bile acid concentration within each group. Most bile acids were expectedly in the free state, only a low percentage in the glycine- or taurine-conjugated form. The sulfated fraction was small and not different in the two groups. Although our data do not refute the hypothesis of bile acids being implicated in the pathogenesis of colorectal cancer, they do not support it.