[Prenatal recording of fetal heart action with magnetocardiography]. / Pränatale Registrierung fetaler Herzaktionen mit Magnetokardiographie.

Fetal magnetocardiography (fMCG) registers the magnetic field generated by the fetal heart. In contrast to the fetal electrocardiogram, fECG permits non-invasive registration of fetal heart activity and documentation of all parts of the PQRST-wave-forms from the second trimenon onwards. This facilitates the determination of cardiac time intervals and establishment of reference values for different stages of pregnancy. We examined 53 women in 104 recordings from the 10th week of gestation onwards (1 to 10 recordings per individual). The fMCG (37 magnetic channels, sampling rate 1024 Hz, bandwidth 1-200 Hz) was recorded non-invasively over the mother's abdomen in a magnetically shielded room. Registration of fetal heart beats was generally successful from the 20/21th week of gestation onwards. In a few cases, fetal heart beats could be registered as early as in the 16th week. Cardiac time intervals and amplitudes of fMCG increased concordantly with fetal growth. Mean P wave duration increased from 31 to 49 ms (p < 0.05), PQ interval from 95 to 107 ms (n.s.) and QRS duration from 36 to 52 ms (p < 0.01). The mean amplitudes of the P and R waves also increased. FMCG, furthermore permits a prenatal diagnosis of fetal cardiac arrhythmias. We recorded fetal arrhythmias in 20 cases (26-38th week), including episodes of ventricular and supraventricular arrhythmias or atrioventricular blockings. Due to its high resolution, fMCG offers new information on the development of fetal cardiac activity which cannot be achieved by conventional methods like cardiotocography or dopplerultrasound. Therefore, fMCG could become a new diagnostic instrument for monitoring fetal wellbeing during pregnancy.

Intragastric pH and serum gastrin during administration of different doses of pantoprazole in healthy subjects.

OBJECTIVE AND DESIGN: The effect of increasing doses of pantoprazole, a newly developed proton pump inhibitor, given at once daily doses of 40, 80 and 120 mg, on intragastric pH and serum gastrin profiles was studied in 15 healthy subjects in a randomized, double-blind, crossover study and compared to recordings without therapy. Measurements of intragastric pH and serum gastrin were performed on the 7th day of treatment by continuous pH recording and radioimmunoassay in blood samples obtained in 1-h intervals, respectively. RESULTS: Pantoprazole significantly increased gastric pH above basal at all pantoprazole doses studied: median 24-h pH rose from 1.2 without therapy to 3.4, 3.3 and 3.6 at 40, 80 and 120 mg daily, respectively. The corresponding integrated 24-h gastrin output was 1632, 2338 and 2248 pg/ml x 24 h compared to 575 pg/ml x 24 h without pantoprazole. There was no interindividual correlation between values of 24-h median pH and 24-h gastrin output at any pantoprazole dose studied. However, fasting gastrin levels closely correlated with 24-h gastrin output (r = 0.789; P < 0.0001). The acid inhibitory effect was significantly (P < 0.01) augmented in Helicobacter pylori positive subjects. CONCLUSION: It is concluded that pantoprazole is an effective inhibitor of gastric acid secretion. Increasing a single pantoprazole dose above 40 mg does not lead to increased median pH elevation. The individual extent of acid inhibition does not predict the magnitude of gastrin elevation. Acid inhibition appears more efficient in Helicobacter pylori positive subjects.

Behavior of the basement membrane during carcinoma cell invasion in chemically induced carcinomas of the skin.

Immunohistochemical localizations of the intrinsic basal lamina (BL) components laminin-1 and type IV collagen, the adhesion molecules type VII collagen and laminin receptor (alpha 6 beta 1 integrin), and the type IV collagenase (72 kDa, MMP2) were analyzed in carcinomas of the mouse skin which were chemically induced by benzo[a]pyrene with or without the addition of the promotor phorbol 12-myristate 13-acetate. Normal skin, dysplastic lesions, and invasive carcinomas were investigated by histological and immunohistochemical (immunofluorescence and APAAP) methods. A regular and continuous staining of laminin-1 and type IV collagen was present in the normal skin and in areas of slight and moderate dysplasia. Underneath highly dysplastic epithelium, the BL became thin, loosened and sometimes disrupted, and accumulations of globular BL material were found in the connective tissue underneath the BL. Type VII collagen retained a more linear, continuous and uniform distribution in the areas of progressed epithelial dysplasia. All invasive carcinomas were characterized by a BL which was disrupted by gaps of varying size but, again, showed a more uniform and less discontinuous distribution of the anchoring molecule type VII collagen. Expression of the integrin laminin receptor investigated increased quantitatively in dysplastic lesions and in areas of invasive carcinomas, showing a circular presence at the surface of most epithelial cells of the basal and spinous layers of the epidermis, whereas, in the normal skin, the laminin receptor was polarized to the basal and lateral cell membrane of basal epithelial cells in contact with the BL. These results suggest that the discontinuities occurring in the BL during carcinoma cell invasion are not caused by a local loss of the anchoring molecules type VII collagen and/or laminin receptor, though alterations in the pattern of expression of the laminin receptor document fundamental changes in the cellular organization occurring during malignant transformation. On the other hand, the presence of the type IV collagenase increased in epithelial dysplasias and invasive carcinomas. In many dysplastic lesions, it was deposited in a plaque-like and sometimes linear manner near the basement membrane (BM) region indicating that, in chemically induced carcinomas, this enzyme may be involved in the process of BM perforation during carcinoma cell invasion.

The basement membrane and its involvement in carcinoma cell invasion.

During the development of invasive cancer, carcinoma cells have to penetrate the extracellular matrix including the basement membrane (BM). This is a usually continuous layer composed of a dense meshwork of collagens, glycoproteins and proteoglycans. It normally underlies epithelia and lacks any pores large enough to allow epithelial cells to pass through them. In consequence, the invasion of carcinoma cells through the BM must be either an active process effected by the carcinoma cells themselves or is mediated by structural alterations of the BM occurring during carcinogenesis and cancer progression. It was supposed by many authors that invading and metastasizing carcinoma cells are able to degrade actively the continuous, uninterrupted BM by secreting type IV collagenase and other proteolytic enzymes. Although there is a wealth of experimental evidence which fits the concept that the active degradation of the BM is an essential requirement for carcinoma cell invasion and metastasis, certain data do not agree with this hypothesis. Thus, it is still doubtful whether active lysis of the BM by carcinoma cells is actually a prerequisite for invasion and metastasis or whether there are alternative and/or additional mechanisms favoring the invasion of carcinoma cells.