Search PubMed⌕ Search

Biomedical subjects

P Kaufmann

Publications and source records attributed to P Kaufmann.

At least 109 records · Page 6Linked to original sources
PubMed1996

Mitochondrial DNA and RNA processing in MELAS.

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), a maternally inherited disorder, is usually associated with a point mutation in mitochondrial DNA (mtDNA) at position 3,243 in the tRNA Leu(UUR) gene. To further study the pathogenesis of MELAS, we analyzed tissues from 8 MELAS-3,243 patients. Southern blot analysis showed an increase in the ratio of mtDNA to nuclear DNA in almost all tissues examined, implying that mitochondrial proliferation is ubiquitous and is not confined to ragged-red fibers in muscle. By northern blot analysis, we demonstrated increased steady-state levels of RNA 19, a polycistronic transcript corresponding to the 16S rRNA + tRNA Leu(UUR) + ND1 genes (which are contiguous in the mtDNA) in heart, kidney, and muscle. These results provide further evidence that altered mitochondrial nucleic acid metabolism may have pathogenic significance in MELAS.

Adult↗
PubMed1996

Diagnostic guidelines in central nervous system Whipple's disease.

Many cases of central nervous system (CNS) Whipple's disease are not diagnosed until postmortem. Few reviews of CNS Whipple's disease have delineated the frequencies of abnormalities on neurological examination, cerebrospinal fluid studies, neuroimaging, and intestinal biopsy studies. Guidelines for diagnosis and treatment have not been proposed. In this review we present 3 new cases of CNS Whipple's disease and summarize the literature to determine the frequencies of neurological signs and abnormalities on diagnostic testing. We propose guidelines for diagnostic screening, selection for biopsy, and treatment. Review of the 84 cases of CNS Whipple's disease (81 in the literature, 3 new) revealed that 80% of the patients had systemic signs. Cognitive changes were frequent (71%), and 47% with cognitive changes also had psychiatric signs. Oculomasticatory myorhythmia and oculo-facial-skeletal myorhythmia, pathognomic for CNS Whipple's disease, were present in 20% of patients, and were always accompanied by a supranuclear vertical gaze palsy. Tissue biopsy was a sensitive technique; 89% of those who had biopsies had positive biopsy results. Diagnosis and treatment of definite CNS Whipple's disease should be based on the presence of pathognomic signs (oculomasticatory myorhythmia or oculo-facial-skeletal myorhythmia) or positive biopsy or polymerase chain reaction results. Possible CNS Whipple's disease should be diagnosed in the setting of unexplained systemic symptoms and neurological signs (supranuclear vertical gaze palsy, rhythmic myoclonus, dementia with psychiatric symptoms, or hypothalamic manifestations). Those with possible CNS Whipple's disease should undergo small-bowel biopsy.

Anti-Bacterial Agents↗
PubMed1996

Placental villous stroma as a model system for myofibroblast differentiation.

Different subtypes of myofibroblasts have been described according to their cytoskeletal protein patterns. It is quite likely that these different subtypes represent distinct steps of differentiation. We propose the human placental stem villi as a particularly suitable model to study this differentiation process. During the course of pregnancy, different types of placental villi develop by differentiation of the mesenchymal stroma surrounding the fetal blood vessels. In order to characterise the differentiation of placental stromal cells in the human placenta, the expression patterns of the cytoskeletal proteins vimentin, desmin, alpha- and gamma-smooth muscle actin, pan-actin, smooth muscle myosin, and the monoclonal antibody GB 42, a marker of myofibroblasts, were investigated on placental tissue of different gestational age (7th-40th week of gestation). Proliferation patterns were assessed with the proliferation markers MIB 1 and PCNA. Additionally, dipeptidyl peptidase IV distribution was studied in term placenta and the ultrastructure of placental stromal cells was assessed by electron microscopy. Different subpopulations of extravascular stromal cells were distinguished according to typical co-expression patterns of cytoskeletal proteins. Around the fetal stem vessels in term placental villi they were arranged as concentric layers with increasing stage of differentiation. A variable layer of extravascular stromal cells lying beneath the trophoblast expressed vimentin (V) or vimentin and desmin (VD). They were mitotically active. The next layer co-expressed vimentin, desmin, and alpha-smooth muscle actin (VDA). More centrally towards the fetal vessels, extravascular stromal cells co-expressed vimentin, desmin, alpha- and gamma-smooth muscle actin, and GB 42 (VDAG). Cells close to the fetal vessels additionally co-expressed smooth muscle myosin (VDAGM). Ultrastructurally, V cells resembled typical mesenchymal cells. VD cells corresponded to fibroblasts, while VDA and VDAG cells developed features of myofibroblasts. Cells of the VDAGM-type revealed a smooth muscle cell-related ultrastructure. In earlier stages of pregnancy, stromal cell types with less complex expression patterns prevailed. The media smooth muscle cells of the fetal vessels showed a mixture of different co-expression patterns. These cells were separated from extravascular stromal cells by a layer of collagen fibres. The results obtained indicate a clearly defined spatial differentiation gradient with increasing cytoskeletal complexity in human placental stromal cells from the superficial trophoblast towards the blood vessels in the centre of the stem villi. The spatial distribution of the various stages of differentiation suggests that human placental villi could be a useful model for the study of the differentiation of myofibroblasts.

Biomarkers↗
PubMed1996

Extracellular matrix components of the placental extravillous trophoblast: immunocytochemistry and ultrastructural distribution.

Invasive extravillous trophoblast cells of the human placenta are embedded in a self-secreted extracellular matrix, the matrix-type fibrinoid. The ultrastructure and molecular composition of the matrix-type fibrinoid of the term human placenta were studied by transmission electron microscopy and immunogold labelling. We used antibodies directed against different matrix proteins such as collagen type IV, laminin, vitronectin, heparan sulfate, various fibronectin isoforms, and against the oncofetal blood group antigen, "i". Immunogold labelling patterns of matrix proteins are the basis for the subdivision of the trophoblast-derived matrix-type fibrinoid into mosaic-like patches of structurally and immunocytochemically different compartments. Firstly, fine granular patches with structural similarities to basal lamina material are composed solely of collagen type IV and laminin. Secondly, an ultrastructurally amorphous glossy substance shows reactivity with antibodies against heparan sulfate and vitronectin. A third type of patches, fine fibrillar networks embedded in the above-mentioned glossy matrix, are reactive with antibodies against normal fibronectin isoforms (IST-4, IST-6, IST-9) and oncofetal isoforms (BC-1, FDC-6). The blood group precursor antigen "i" was not only expressed on the surfaces of the extravillous trophoblast cells but was associated with the fibronectin-positive fibrils. In conclusion, within this extracellular matrix, clear compartments of different composition can be distinguished from each other. Glycosylation with "i" in this matrix may be involved in immunological masking, thus preventing rejection of placenta and fetus.

Antibodies↗
PubMed1996

Coronary artery dimensions in primary and secondary left ventricular hypertrophy.

BACKGROUND: Coronary artery enlargement has been previously described in left ventricular hypertrophy. OBJECTIVES: We sought to assess coronary artery dimensions and their relation to left ventricular muscle mass in primary and secondary hypertrophy. METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease). As a measure of left ventricular hypertrophy, angiographic left ventricular mass and equatorial cross-sectional muscle area were determined. RESULTS: Cross-sectional area of both the left and right coronary arteries is increased in left ventricular hypertrophy (p < 0.05 vs. values in control subjects). There is a curvilinear relation between left coronary artery size and left ventricular muscle mass (r = 0.76) or cross-sectional muscle area (r = 0.75). However, normalization of coronary cross-sectional area for left ventricular muscle mass or muscle area shows insufficient enlargement of the coronary arteries in both primary and secondary hypertrophy. CONCLUSIONS: 1) Coronary artery size increases as left ventricular mass increases in both primary and secondary hypertrophy. 2) The enlargement of left coronary cross-sectional area is independent of the cause of the increase in left ventricular mass. 3) The size of the coronary arteries is inappropriate with regard to left ventricular hypertrophy. Thus, the stimulus for growth of the coronary arteries is not influenced by the underlying disease but appears to depend on the degree of left ventricular hypertrophy.

Adult↗
PubMed1996

Structural analysis of placental terminal villi from growth-restricted pregnancies with abnormal umbilical artery Doppler waveforms.

The abnormal umbilical artery Doppler waveform represented by absent end-diastolic flow velocity (AEDFV) identifies a group of preterm small-for-gestational age fetuses that are at high risk of perinatal death due to chronic fetal hypoxia. The placental ischaemia that results from inadequate trophoblast invasion of spiral arterioles leads to an assumption of placental villous hypoxia, though an alternative explanation is that the placenta fails to adequately transfer oxygen to the fetus from the intervillous space. Because oxygen transport takes place within the terminal villi, we undertook the first detailed studies of villous ultrastructure structure and immunohistochemistry in order to determine the likely origin of fetal hypoxia in this condition. Terminal villi were examined ultrastructurally using transmission electron microscopy and by immunohistochemical localization of matrix molecules (laminin and collagens I, III and IV) and a marker of cell proliferation (MIB-1), in 16 small-for-gestational age pregnancies with AEDFV in the umbilical artery [deemed to have intrauterine growth restriction (IUGR)] and in 16 gestation age-matched controls. Terminal villi from the IUGR cases were smaller in diameter (P < 0.02) and had several abnormal features in comparison with the controls; increased syncytial nuclei (P < 0.01), reduced cytotrophoblast nuclei (P < 0.01), thickened basal lamina (P < 0.01), and increased stromal deposition of collagens and laminin. The amount of proliferating cytotrophoblast was reduced in the IUGR group (P < 0.014) and the degree of capillary erythrocyte congestion within terminal villous capillaries was increased (P < 0.001). Several of the structural differences in the terminal villi of the IUGR group such as reduced cytotrophoblast proliferation and stromal fibrosis are incompatible with the prevailing view of placental hypoxia in IUGR. Rather thickening of the basal lamina and congestion of the capillaries by erythrocytes are predicted to limit oxygen transfer from the intervillous space to the fetus and may represent an equilibration of oxygen tension between intervillous space and the terminal villi. Despite the known reduction in uteroplacental blood flow in IUGR, fetoplacental blood flow is compromised to a far greater extent in the presence of AEDFV such that maternal blood leaving the placenta has a higher oxygen content than under normal circumstances.

Biological Transport↗
PubMed1996

Increased plasma concentrations of circulating intercellular adhesion molecule-1 (cICAM-1) in patients with necrotizing pancreatitis.

The intercellular adhesion molecule-1 (ICAM-1), a membrane glycoprotein, is important in the adhesion of cytokine-stimulated leukocytes to the endothelium of microvessels and their transendothelial migration. Circulating isoforms of ICAM-1 (cICAM-1) are known to be elevated in human serum as an indirect consequence of inflammatory responses. The aim of this study was to investigate whether cICAM-1 levels are elevated in patients with acute pancreatitis within 48 h of the onset of abdominal pain and whether cICAM-1 levels correlate with the severity of the tissue damage. Twenty-five consecutive patients admitted to a medical ICU had elevated cCAM-1 concentrations of 548 +/- 68 ng/ml, significantly different when compared to a control group of 18 healthy subjects (343 +/- 29; p = 0.018). According to the findings of contrast-enhanced CT or laparotomy patients were further divided in a group with acute edematous pancreatitis and a group with acute necrotizing pancreatitis. Pancreatic necrosis was associated with cICAM-1 levels of 729 +/- 106 ng/ml, significantly different from patients with mild disease (367 +/- 48) and controls (p < 0.001). Plasma cICAM-1 levels were not significantly different between healthy subjects and patients with mild pancreatitis. A significant correlation was found between cICAM-1 and C-reactive protein, an acute phase reactant and marker of necrotizing pancreatitis (r = 0.62; p < 0.01). The sensitivity and specificity for the detection of edematous or necrotizing pancreatitis of cICAM-1 plasma concentrations (cutoff point at 500 ng/ml) were 75% and 85%, respectively. These results suggest an enhanced release of ICAM-1 into plasma in the early stage of acute necrotizing pancreatitis. Leukocyte-endothelial cell adhesion may be associated with the inflammatory process of necrotizing tissue damage in acute pancreatitis. It could thus serve as a marker or predictor of a severe clinical course of pancreatitis.

Adult↗
PubMed1996

Abnormal coronary vasomotion in hypertension: role of coronary artery disease.

OBJECTIVES: This study sought to evaluate the effect of dynamic exercise on coronary vasomotion in hypertensive patients in the presence and absence of coronary artery disease. BACKGROUND: Endothelial dysfunction with abnormal coronary vasodilation in response to acetylcholine has been reported in patients with arterial hypertension. METHODS: Coronary artery dimensions of a normal and stenotic vessel segment were determined in 64 patients by biplane quantitative coronary arteriography at rest and during supine bicycle exercise. Patients were classified into two groups: 20 patients without evidence of coronary artery disease (10 normotensive, 10 hypertensive [group 1]) and 44 patients with coronary artery disease (26 normotensive, 18 hypertensive [group 2]). Both groups were comparable with regard to clinical characteristics, serum cholesterol levels, body mass index, exercise capacity and hemodynamic data. RESULTS: Mean aortic pressure was significantly higher in hypertensive than normotensive patients. Exercise-induced vasodilation of the normal vessel segment was similar in normotensive and hypertensive patients without coronary artery disease (group 1), namely, +19% versus +20%. However, in hypertensive patients with coronary artery disease, exercise-induced vasodilation was significantly less in both normal and stenotic vessel segments than in normotensive subjects (+1% vs. +20% for normal [p < 0.003] and -20% vs. -5% for stenotic vessels [p < 0.025]). Administration of 1.6 mg of sublingual nitroglycerin at the end of exercise led to a normalization of the vasodilator response in normotensive as well as hypertensive patients. However, this response became progressively abnormal in group 2 when coronary artery disease was present. CONCLUSIONS: In the absence of coronary artery disease, the vasomotor response to exercise is normal in both normotensive and hypertensive patients. However, in hypertensive patients with coronary artery disease, an abnormal response of the coronary vessels can be observed, with a reduced vasodilator response to exercise in normal arteries but an enhanced vasoconstrictor response in stenotic arteries. This behavior of the epicardial vessels during exercise suggests the occurrence of endothelial dysfunction (i.e., functional defect) that is not evident in the absence of coronary artery disease. Nitroglycerin reverses impaired coronary vasodilation, but this effect is blunted in the presence of coronary artery disease (i.e., structural defect).

Coronary Angiography↗
PubMed1996

The fibrinoids of the human placenta: origin, composition and functional relevance.

Placental fibrinoids are extracellularly deposited materials which are histologically glossy and acid staining, and can be found in every normal and pathological placenta at all stages of pregnancy. The amount of fibrinoid is, in general, independent of pregnancy outcome and fetal wellbeing. According to new findings, the classical histological term "fibrinoid" covers two distinctive extracellular matrices which differ as regards structure, composition and function. Fibrin-type fibrinoid is mostly composed of fibrin together with other molecules derived from blood clotting or degenerative processes. It is mainly a maternal blood-clot product which is used (a) to adapt the intervillous space to optimized flow conditions and (b) to control growth of the villous trees by encasing new villous branches which caused intervillous stasis or turbulence of maternal blood. Moreover, fibrin-type fibrinoid replaces degenerative syncytiotrophoblast at the maternofetal exchange surfaces, thus acting as a kind of substitute barrier. Matrix-type fibrinoid is a secretory product of invasive extravillous trophoblast cells. It shares some similarities with basement membranes, however, it is secreted in an apolar fashion, embedding the secreting cells. Like basement membranes, it contains laminins, collagen IV, and heparan sulfate. In addition, oncofetal fibronectins, vitronectin, and i-glycosylated molecules but no collagens I, III, and VII can be found. Matrix-type fibrinoid is thought to regulate trophoblast invasion by specific interactions with cell surface integrins. As a kind of "glue", it anchors the placenta to the uterine wall and seems to play an important role in materno-fetal immune interactions at this particular site. Both types of fibrinoid are usually co-localized, thus indicating close morphogenetic and functional interrelations.

Animals↗
PubMed1996

Intensive care management of acute pancreatitis: recognition of patients at high risk of developing severe or fatal complications.

The clinical spectrum of acute pancreatitis ranges from mild, self-limiting disease of fulminant illness that may rapidly lead to multiple organ failure and death. To identify factors associated with a subsequent severe course and/or high mortality we investigated retrospectively 91 patients admitted to the medical intensive care unit (ICU) with acute pancreatitis during a 2 year period. 67% of the attacks were mild (< or = 1 complication). The overall mortality rate was 9%, whereby 3% of patients with alcoholic and 13% with biliary pancreatitis died. 75% of the patients in the group with a fatal outcome were aged over sixty and 30% in the group with a mild course (p < 0.05). Females with pancreatitis of biliary origin had a mild course in 57% and a severe (> or = 2 complications) or fatal outcome in 43%. In males with alcohol abuse we observed a mild form of pancreatitis in 79% and a severe or fatal course in 21%. The delay between onset of abdominal pain and commencement of treatment in hospital was greater than 12 hours in 70% of all patients studied and there was no association with severity and development of subsequent complications. The median of the acute physiology and chronic health evaluation scoring system (APACHE-III) on the day of admission was 19 in patients with mild disease, which was significantly lower than in patients with severe (40) or fatal acute pancreatitis (53) (p < 0.0001). Serial APACHE-III measurements over 5 days after admission provided further differentiation between mild and severe or fatal cases (p < 0.0001), but no significant difference was observed between survivors with severe course and fatal outcome. In addition, RANSON scores were calculated for comparison with APACHE-III at admission and after 48 hours: concerning the recognition between mild and severe/fatal pancreatitis both scoring systems exhibited similar significant differences on day 1 and day 2. The RANSON scoring system provided further a significant differentiation between survivors with a severe course of pancreatitis when compared to deaths on day 2, whereas the APACHE-III scoring system did not. Advanced age, female sex, biliary obstruction and elevated RANSON and APACHE-III scores are risk factors for an increased rate of life-threatening complications in acute pancreatitis. The daily assessment of such scoring systems may allow the recognition of such patients and may be helpful in the routine clinical management and monitoring of acute pancreatitis.

APACHE↗
PubMed1996

Technetium-99m-sestamibi uptake in breast tumor and associated lymph nodes.

UNLABELLED: The aim of this study was to measure the accumulation of 99mTc-sestamibi in breast tumors and their axillary lymph nodes in patients undergoing scintimammography. METHODS: Eighteen patients who were scheduled for breast surgery underwent scintimammography with 740 MBq of 99mTc-sestamibi on the day before the operation. The next morning, reinjection with 370 MBq was performed. Immediately after the surgical procedure, the 99mTc activity of the tumor samples and, when available, the related lymph nodes was measured in a gamma counter. The samples were weighed and prepared for histological analysis. The activity of each sample was normalized to the mean activity of normal tissue samples obtained from the same patient. RESULTS: Among the 198 samples analyzed, the relative uptake of sestamibi was increased in 111 containing normal lymph nodes (1.80+/-0.79 vs 1.00+/-0.22, p<0.05), as well as in the seven containing invaded lymph nodes (2.01+/-0.83, p<0.01) and more dramatically, in the 22 with a carcinoma (5.64+/-3.06, p<0.001). In two patients with a benign lesion, both scintigraphy and counting demonstrated increased activity in the tumor. Four patients had negative scan results despite the presence of malignant tumor and a more than fourfold increase of sestamibi concentration in two of them. CONCLUSION: Technetium-99m-sestamibi concentrates strongly in breast carcinoma, sometimes even when the scan results appear normal, and mildly in lymph nodes, especially when invaded; it also concentrates in some benign tumors, possibly in relation to the presence of epithelial hyperplasia.

Adult↗
PubMed1996

[Smoking behavior and views on the smoking topic in the Styrian population--results of a survey at the Graz autumn convention].

Cigarette smoking has been identified as a major risk factor for cardiovascular diseases apart from hypercholesterolemia and arterial hypertension. Diseases of the respiratory system and several neoplasms as well as complications of pregnancy are considered to be "smoking-related", too. In order to survey the smoking habits and views on smoking in the Styrian population, a questionnaire was issued to 1034 visitors of the Graz Autumn Fair 1992. Pleasure proved to be the main motivation for smoking both in men and in women, habit, addiction, stress and boredom being further motivations. Not only non-smokers, but also smokers were assessed to be aware of smoking being a health hazard. Prohibition of tobacco advertising was accepted most widely as a mean of anti-smoking campaign. About half the non-smokers are exposed to environmental tobacco smoke, at place of work more frequently than at home. Percentage of smokers differs with age and job classes, however, no geographical variations were found. Further anti-smoking measures should be considered. Smoking restrictions at place of work and in public could prevent passive smoking. Ban on advertising seems to be the most effective anti-smoking campaign.

Adolescent↗
PubMed1995

Reduced epicardial coronary vasodilator capacity in patients with left ventricular hypertrophy.

BACKGROUND: Enlargement of the epicardial coronary arteries occurs in left ventricular (LV) hypertrophy as an adaptation to the increased coronary blood flow. METHODS AND RESULTS: Vasodilator capacity of the epicardial coronary arteries was determined in 44 patients. The dose-response relation of intracoronary nitroglycerin was assessed in 14 patients (7 control subjects and 7 patients with aortic stenosis [study A]) using quantitative coronary angiography. In a second study (B), vasodilator capacity of the epicardial coronary arteries was determined in 15 control subjects and 15 patients with valvular heart disease. In study A, a curvilinear dose-response relation with maximal vasodilation after 90 micrograms intracoronary nitroglycerin was found in both control subjects and patients with aortic stenosis. Vasodilator capacity was reduced in those with aortic stenosis, although sensitivity to nitroglycerin was similar in both groups. In study B, coronary circumferential length at baseline was larger in those with LV hypertrophy (12.2 +/- 2.2 mm) than in control subjects (8.6 +/- 1.5 mm; P < .001); after 100 micrograms intracoronary nitroglycerin, it increased to 12.9 +/- 2.2 mm (6 +/- 5%) in those with LV hypertrophy and to 10.3 +/- 1.5 mm (21 +/- 8%; P < .001) in control subjects. An inverse relation between baseline circumferential length and its percent increase after nitroglycerin was found (r = -.71, P < .001). CONCLUSIONS: Vasodilator capacity of the epicardial coronary arteries is reduced in patients with LV hypertrophy, although sensitivity to nitroglycerin is normal. This may be due to a flow-mediated decrease in coronary vasomotor tone and/or the occurrence of vascular remodeling with an enlargement of the coronary arteries.

Adult↗
PubMed1995

Angiotropic large cell lymphoma presenting as thrombotic microangiopathy (thrombotic thrombocytopenic purpura).

BACKGROUND: Angiotropic large cell lymphoma is a rare lymphoproliferative disorder that affects vessels of almost all organs. Therefore, many different signs and symptoms can be observed and may delay a rapid diagnosis in these patients. However, no association between angiotropic large-cell lymphoma and thrombotic microangiopathy (TMA) has been reported so far. METHODS: The case report describes a 69-year-old female Caucasian who presented with fever, neurologic symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and hyaline thrombi within small vessels. TMA was diagnosed and intense treatment, including plasma exchange and corticosteroid therapy, was initiated. Nevertheless, the patient died 3 days after admission. A postmortem examination including immunohistochemistry and molecular studies was performed. RESULTS: Autopsy revealed angiotropic large cell lymphoma with tumor cell aggregates in small vessels of the brain, myocardium, lungs, liver, small and large intestines, mesenterium, kidneys, and lymph nodes. Immunohistochemical analysis of the tumor cells showed positive reactions with B-cell markers, but negative T-cell and epithelial cell markers. Molecular studies using polymerase chain reaction with primers for the rearranged immunoglobulin heavy chain and the T-cell receptor beta chain gene confirmed the diagnosis of a monoclonal B-cell disorder. CONCLUSION: TMA can occur in association with angiotropic large cell lymphoma and, furthermore, can be its sole clinical manifestation.

Aged↗
PubMed1995

Physiological dilation of uteroplacental arteries in the guinea pig depends on nitric oxide synthase activity of extravillous trophoblast.

The trophoblast invasion of uteroplacental arteries in the guinea pig has been studied by means of electron microscopy and immunohistochemisty. To identify trophoblast cells, smooth muscle cells, and endothelial cells, antibodies against cytokeratins, smooth muscle myosin, desmin, and vimentin were employed. Furthermore, the immunohistochemical expression patterns of nitric oxide synthase isoforms (eNOS, mNOS and bNOS) were studied and were compared with the enzyme histochemical staining for NADPH-diaphorase. Dilation of uteroplacental arteries begins prior to day 30, when trophoblast cells that coexpress endothelial and macrophage nitric oxide synthase can be found in the vicinity of the vessels and replace the surrounding peritoneal mesothelium. Trophoblast invasion of the arterial walls and the subsequent wall destruction are only secondary effects. Starting around day 50, the final steps of pregnancy-dependent vessel modifications involve intraarterial trophoblast adhesion to the endothelium and subsequent replacement of the endothelium by the trophoblast cells. These may centrifugally invade the vessel media eventually forming intraluminal plugs. These findings led us to the conclusion that in the guinea pig pregnancy-induced physiological dilation of the uteroplacental arteries is due to the effect of nitric oxide rather than being caused by trophoblast-induced media destruction.

Animals↗
PubMed1995

The monoclonal antibody GB 42--a useful marker for the differentiation of myofibroblasts.

The expression patterns of a variety of cytoskeletal antigens were studied in normal human tissues (placenta, umbilical cord, myometrium, colon, mammary gland, testis, skeletal muscle, myocardium) as well as in abnormal human tissues (palmar fibromatosis, fibrocystic disease of the mammary gland, mammary carcinoma). The immunohistochemical binding patterns of the monoclonal antibody GB 42 were compared to those of commercial antibodies directed against vimentin, desmin, smooth muscle myosin, pan actin, alpha-smooth muscle actin and gamma-smooth muscle actin. Methods applied comprised immunohistochemistry on cryostat sections and paraffin sections. Immunogold immunocytochemistry was performed on Lowicryl sections. The patterns of GB 42-binding were confirmed biochemically by SDS-PAGE and Western-blotting, and quantitative amino acid analysis. Our data suggest that the monoclonal antibody GB 42 recognizes an actin isoform which is identical to, or closely related to, gamma-smooth muscle actin. Unlike the commercially available antibody against gamma-smooth muscle actin, GB 42 does not cross-react with alpha-skeletal or alpha-cardiac actins. The GB 42-antigen is expressed in smooth muscle cells, myoepithelial cells and in later stages of differentiation of myofibroblasts, in all the tissues investigated. Throughout the development of smooth muscle cells and myofibroblasts, the appearance of the GB 42-antigen occurs after the expression of vimentin, desmin and alpha-smooth muscle actin, but prior to the expression of smooth muscle myosin. GB 42 is a reliable marker for higher stages of differentiation of smooth muscle cells and myofibroblasts.

Amino Acids↗