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Biomedical subjects

H Müntefering

Publications and source records attributed to H Müntefering.

At least 37 records · Page 2Linked to original sources

[Pulsed Doppler sonography of the umbilical artery and fetoplacental resistance. A histometric study of gestosis placentas in comparison with a normal sample].

Histometric data from placentas after EPH gestosis, in cases with normal (n = 15) or pathological (n = 13) foetal umbilical artery flow velocity wave forms, are compared with data from uncomplicated pregnancies (n = 17). The cross-sectional areas of the villi were increased in both gestosis groups, whereas the diffusion capacity, the degree of vascularisation, the foetal placental blood volume and the length of epithelial plates and their quota of the circumference of the villi are decreased only in cases of gestosis with pathological flow velocity wave forms. In this group a high rate of caesarean sections for foetal distress was necessary and the foetal outcome was poor. We were able to prove the possibility of estimation of "placental risk" with pulsed Doppler ultrasound of an umbilical artery with morphometric data.

Asphyxia Neonatorum↗

[Doppler sonography of the umbilical artery: differential diagnosis in intrauterine growth retardation].

50 fetuses with IUGR were differenciated by pulsed Doppler-wave velocimetry of an umbilical artery. All cases with a normal A/B-ratio according to Stuart had spontaneous vaginal delivery and normal fetal outcome. Pathological flow velocity waveforms led to early delivery and a significantly high rate of cesarean section for fetal asphyxia and to a poor fetal outcome. The umbilical artery flow velocity waveform showed a high sensitivity and specificity with regard to fetal risk and indicated the latter earlier than the oxytocin challenge test. A positive correlation between elevated umbilical placental resistance and histomorphological disorders of the fetal placenta was found. Screening for fetal perinatal risk by means of pulsed Doppler ultrasound of the umbilical arteries is discussed in cases of IUGR.

Blood Flow Velocity↗

[Is type I diabetes a virus-induced disease?].

The conditions are critically reviewed under which diseases might be aetiologically related to infection by a certain virus. Such a causal correlation has to obey Koch's postulates, but may be very difficult to prove in the case of a "hit and run" process. This will be exemplified in the case of insulin-dependent diabetes mellitus (IDDM). Observations in humans and the results of experiments on laboratory animals are reported, whereby the Coxsackie B and mumps viruses are of particular interest. Furthermore, the mechanisms by which viruses may produce autoimmune diseases are discussed, including virological and immunological aspects. The hypothesis of "molecular mimicry" by Oldstone is quoted as a unifying one, allowing the combination of both aspects. His main assumption is oligopeptide homology between certain virus proteins and some cell proteins and some examples are given. In the presence of such homologies the immune system is first stimulated by the parasitic virus protein, but somewhat later this reaction switches against the host structures, causing continuing cellular damage with the development of autoimmune disease. It is concluded that Koch's postulates in such cases have to be supplemented by assaying for amino acid homologies in viruses and certain cell types.

Animals↗

Encephalomyocarditis virus and diabetes mellitus: studies on virus mutants in susceptible and non-susceptible mice.

The so-called M-variant (especially subtype D) of encephalomyocarditis virus (EMCV) induces a diabetes-like syndrome in certain mouse strains which may serve as a model of insulin-dependent diabetes mellitus (IDDM) in man. The development and course of diabetes was influenced by a number of virus and host factors, among these being virus strain, virus dose, mouse strain, age, sex, and the host's immunological status. In a D-variant stock of EMCV, we found a virus plaque variant (PV 2) diabetogenic for DBA/2 mice, and at least one variant (PV 7) that did not affect carbohydrate metabolism. Although the diabetogenicity of PV 2 proved to be a genetically stable characteristic after further passages in vivo and in vitro, the incidence of diabetes varied somewhat (mean value 65% in 10-week-old DBA/2 mice infected with 10(5) p.f.u.). Both lower (10(1) or 10(3) p.f.u.) and higher (10(7) or 10(8) p.f.u.) virus doses led to a diminished incidence and severity of diabetes. In younger animals (5 weeks) transient hyperglycaemia often appeared, whereas in older animals (20 weeks) there was a higher rate of mortality. Histological examination of the islets of Langerhans in diabetes-susceptible (DBA/2) and resistant (C57BL/6) mice revealed that EMCV-induced hyperglycaemia appeared to develop in parallel to islet cell damage. Even in diabetic animals, some unaffected islets were regularly found. This study demonstrates that EMCV mutants may have completely different biological effects and produce diabetes only in special circumstances. Host factors play a significant role in the development of diabetes.

Age Factors↗

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Pancreatic tissue obtained at subtotal pancreatectomy from 15 infants with persistent hypoglycaemia with hyperinsulinism, and autopsy specimens from 23 age-matched normoglycaemic controls, were studied with morphometric methods after immunocytochemical staining of the four main islet cell types (A, B, D and pancreatic polypeptide cells). In three cases, a focal lesion was detected by gross examination. Macroscopic or microscopic examination did not distinguish the 12 other cases from controls. As found previously, nesidioblastosis was not a specific feature of the pancreas in infantile hypoglycaemia, being observed in age-matched controls as well. In cases with hypoglycaemia the volume density of B cells was not significantly increased; that of the A cells was within normal range. The volume density of pancreatic polypeptide cells was markedly augmented and that of somatostatin cells was significantly decreased. The mean nuclear volume of the B cells was increased by 40% in cases with diffuse changes, but in cases with a focal lesion this increase was restricted to the abnormal area. This finding is of decisive importance for diagnosis and has therapeutic implications. The increase in B-cell nuclear size is thought to reflect an enhanced functional activity of these cells. On the other hand, the figures obtained for the volume density of B and D cells must be viewed with some reservation because degranulation may interfere with accurate detection of these cells.

Cell Count↗

Prenatal diagnosis of neuroblastoma by sonography.

Herein we report the first case in the literature in which a neuroblastoma in a fetus was recognized before birth and its growth could be observed. The diagnosis was made by ultrasonography. Other helpful diagnostic procedures in prenatal diagnosis are: determination of catecholamines, sonographic examination of the placenta, and search for metastases. As more and more centers perform ultrasound examinations routinely in pregnancy, similar findings such as fetal tumors or congenital malformations are to be expected more frequently.

Adrenal Gland Neoplasms↗

Iatrogenic, insulin-dependent, local amyloidosis.

Human and experimental amyloidosis can occur either as a generalized widespread deposit of various proteins or a localized deposit. We looked for local amyloidosis caused iatrogenically under clinical and experimental conditions. Subcutaneous tissue from one diabetic patient and six Wistar rats, which had received a continuous local infusion of 1.2 iu of insulin daily for 6 weeks, was examined histologically. In all cases the development of granulation tissue around the tip of the catheter was observed. In addition, inhomogenous extracellular deposits showing green birefringence under polarized light when stained Congo red were seen. Immunohistologically, they displayed binding of anti-insulin antibody. Electron microscopy demonstrated a typical spear-like fibrillar structure with a fibril diameter of 60 to 80 A. These findings confirmed that the deposited substance was amyloid. Iatrogenically administered protein produced in vivo amyloidosis at the site of its entry. Insulin can lead to the formation of amyloid fibrils not only in vitro but also in vivo.

Amyloid↗