Collagen membrane/fleece composite film reduces adhesions in the presence of bleeding in a rabbit uterine horn model.

OBJECTIVE: Determination of efficacy in presence of bleeding of CDS, a collagen/membrane fleece composite, in a rabbit uterine horn simple abrasion model. DESIGN: Randomized, controlled, and blinded study involving standard abrasion of the uterine horns with induction of moderate mesouterine bleeding. SETTING: Research laboratory. PATIENT(S): New Zealand White rabbits. INTERVENTION(S): No treatment (surgical control), CDS film, or INTERCEED barrier (negative reference control). MAIN OUTCOME MEASURE(S) AND RESULT(S): The extent (percent length uterine horn) with adhesions was assessed after 29 or 30 days. Adhesions formed in surgical controls to an extent (85.6% +/- 4.6%) consistent with historic data for this model. INTERCEED failed to reduce adhesions (78.1% +/- 7.7%) indicating that the test conditions of inadequate hemostasis were validated. CDS film, despite this inadequate hemostasis, reduced the extent of adhesions (31% +/- 7.4%; P<.01). Both the tenacity (P=.0008) and degree of uterine convolution (P=.000003) was reduced by CDS film but not by INTERCEED. CONCLUSION(S): Under conditions of inadequate hemostasis CDS effected a reduction in adhesion development. CDS may be useful adjuvant for procedures where hemostasis is difficult to achieve.

Human plasma albumin transports [13C]docosahexaenoic acid in two lipid forms to blood cells.

Docosahexaenoic acid (22:6) decreases blood platelet function and is highly concentrated in the brain where its depletion leads to functional impairments. Because the platelets and blood brain barrier capillary endothelium cannot hydrolyze the complex lipids for fatty acid (FA) uptake, nonesterified FA (NEFA) bound to albumin are assumed to be the delivery route of FA to these cells. The supply of 13C-labeled 22:6 to blood cells by plasma albumin was studied in humans after a single ingestion of this FA esterified in a triglyceride (TG). The 22:6 13C/12C ratio, measured by gas chromatography combustion-isotope ratio mass spectrometry was measured in lipid classes from albumin, platelets, leukocytes, and erythrocytes (taken as a tentative index of the brain uptake). Nonesterified [13C]22:6 bound to albumin was rapidly produced after ingestion, as a result of the hydrolysis of very low density lipoprotein (VLDL) plus chylomicron TG. We found that albumin carried another source of 22:6, lyso-phosphatidylcholines (lyso-PC), in which [13C]22:6 accumulated while the nonesterified [13C]22:6 reached its minimal plasma concentrations. Computation of the relative contribution of NEFA and lyso-PC for the [13C]22:6 delivery to platelets and erythrocytes showed that the [13C]22:6 supply to platelets occurred uniquely through NEFA, whereas this pool was weakly involved in the delivery to erythrocytes. In contrast, lyso-PC was uniquely concerned with the 22:6 delivery to erythrocytes and represented the major part of this supply. We conclude that plasma albumin carries 22:6 in two lipid forms that are involved differently in the delivery of this FA to target cells.

Ontogeny of somatostatin binding sites in respiratory nuclei of the human brainstem.

The ontogeny of somatostatin binding sites was studied in 16 respiratory nuclei of the human brainstem, from 19 postconceptional weeks to 6 months postnatal, by quantitative autoradiography using [(125)I-Tyr0,DTrp8]S14 as a radioligand. In the early gestational stages (19-21 postconceptional weeks), moderate to high concentrations of [(125)I-Tyr0,DTrp8]S14 binding sites were found in all nuclei, the highest density being measured in the locus coeruleus. From 19 weeks of fetal life to 6 months postnatal, a decrease in the density of labeling was observed in all nuclei. The most dramatic reduction in site density (80-90%) was found in the ventral part of the nucleus medullae oblongata lateralis and in the nucleus paragigantocellularis lateralis. A 70-80% decrease was detected in the dorsal part of the nucleus tractus solitarius, the nucleus nervi hypoglossi, the ventral part of the nucleus medullae oblongatae centralis, the nucleus ambiguus, the nucleus paragigantocellularis dorsalis, and the nucleus gigantocellularis, and a 60-70% decrease in the nucleus parabrachialis medialis, the ventrolateral and ventromedial parts of the nucleus tractus solitarius, and the nucleus praepositus hypoglossi. A 50-60% decrease was observed in the caudal part of the nucleus tractus solitarius, the nucleus dorsalis motorius nervi vagi, and the nucleus parabrachialis lateralis, whereas in the nucleus locus coeruleus, the concentration of recognition sites decreased by only 30%. The profiles of the decrease in site density differed in the various structures. In the majority of the nuclei, a gradual diminution of binding density was observed either throughout the developmental period studied or mainly during fetal life. Conversely, in two nuclei, i.e., the nucleus parabrachialis lateralis and the locus coeruleus, an abrupt decrease occurred around birth. The differential decrease in the density of somatostatin binding sites observed in respiratory nuclei during development, together with the observation that microinjection of somatostatin in some of these nuclei causes ventilatory depression and apnea, strongly suggests that the somatostatinergic systems of the human brainstem are involved in the maturation of the respiratory control.

Retroconversion and metabolism of [13C]22:6n-3 in humans and rats after intake of a single dose of [13C]22:6n-3-triacylglycerols.

The apparent retroconversion of docosahexaenoic acid (22:6n-3) to eicosapentaenoic acid (20:5n-3) and docosapentaenoic acid (22:5n-3) was studied in vivo, in rats and humans, after they ingested a single dose of triacylglycerols containing [13C]22:6n-3 ([13C]22:6-triacylglycerol), without 22:6n-3 dietary supplementation. The amount of apparent retroconversion and the distribution of the three n-3 polyunsaturated fatty acids (PUFAs) in plasma lipid classes were followed as a function of time by measuring the appearance of 13C in these PUFAs with gas-chromatography combustion-isotope ratio mass spectrometry. This [13C]22:6n-3 retroconversion, calculated by summing the amounts of [13C]22:5n-3 and [13C]20:5n-3 in plasma lipids, was lower in humans than in rats, reaching a maximum of approximately 9% of the total plasma [13C]22:6n-3 in rats, but only 1.4% in humans. The incorporation of [13C]22:6n-3 and [13C]22:5n-3 in lipid classes followed their endogenous distribution with a maximal accumulation in phospholipids, but a low incorporation into cholesterol esters (CEs), whereas [13C]20:5n-3 was equally present in phospholipids and CEs. The ratio of the amount of HDL-CE to HDL-phosphatidylcholine for [13C]20:5n-3 was higher than for [13C]22:6n-3, indicating a selectivity of the lecithin-cholesterol acyltransferase enzyme with regard to these PUFAs, which may be related to the differences in their biological properties after fish oil feeding. The occurrence of a weak basal 22:6n-3 retroconversion in humans supports feeding this pure PUFA in cases in which 20:5n-3 presents undesirable side effects and when specific alterations of blood lipids are expected.

Distribution of somatostatin receptors in the adult human brainstem.

The neuropeptide somatostatin is widely distributed in the central nervous system of rat and human. Somatostatin-containing neurons are particularly abundant in the hypothalamus, the cerebral cortex and the limbic system. Somatostatin is also present in a number of discrete structures in the brainstem and spinal cord. The localization of somatostatin receptors provides valuable information regarding the possible roles of the peptide in the brain. In the present study, we have investigated the precise distribution of somatostatin binding sites in the human lower brainstem by quantitative autoradiography, using [125I- Tyr0,DTrp8]S14 as a radioligand. The tissues were collected from two individuals, aged 50 and 67 years, who had no antecedent of neurological disorders. The binding of the radioligand was visualized in 73 distinct anatomical regions of the medulla and pons and quantified by computer-assisted image analysis. Somatostatin binding sites were present in sensory nuclei, the highest densities being observed in the trigeminal complex (spinalis oralis and interpolaris) and in the nucleus (N.) tractus solitarii. Moderate to low densities of binding sites were detected in the N. vestibularis medialis and spinalis, and in the N. nervus trigemini sensibilis principalis. Many relay nuclei of the ascending somatosensory pathways contained moderate to high densities of binding sites: the inferior olivary complex, the N. arcuatus and the N. praepositus hypoglossi. Binding sites were also present in several motor nuclei such as the N. nervi hypoglossi, the N. dorsalis motorius nervi vagi, the N. nervi facialis and the N. nervi abducentis. Moderate to low concentrations of binding sites were detected in nuclei related to the reticular formation including the N. raphae pallidus, the N. parabrachialis and the N. supratrochlearis. The N. locus coeruleus exhibited a very high concentration of somatostatin binding sites in both individuals. The present data, together with previous studies on the distribution of somatostatin-immunoreactive fibers in the human brainstem, suggest that somatostatin may be involved in (i) sensory processes including vestibular sensitivity, somatosensoriality and proprioception, (ii) sleep-waking cycle and arousal and (iii) control of various neurovegetative functions including regulation of cardiovascular and respiratory activities as well as gastric acid secretion.

Anatomical distribution of somatostatin receptors in the brainstem of the human fetus.

The distribution of somatostatin binding sites was studied in the pons and medulla oblongata of three human fetuses (gestional ages 26, 28 and 30 weeks). The study was carried out by in vitro quantitative autoradiography using either [125I-Tyr0,D-Trp8]somatostatin-14 or [125I-Tyr11]somatostatin-14 as radioligands. Somatostatin binding sites were observed in a number of nuclei subserving sensory, motor or integrative functions within the pons and medulla. In addition, discrete tracts also contained significant amounts of binding sites. Among structures involved in sensory processes, a high density of binding sites (40-60 fmol/ mg wet tissue) was measured in the dorsal cochlear nucleus and in the nucleus tractus spinalis trigemini caudalis. Moderate to high levels of binding sites (30-40 fmol/mg wet tissue) were detected in the other sensory cranial nerve nuclei. A moderate density of sites (15-30 fmol/mg wet tissue) was measured in most motor nuclei, the highest concentrations being observed in the dorsal motor nucleus of the vagus nerve, the facial nucleus, the hypoglossal nucleus and the nucleus ambiguus. The griseum pontis and the nucleus corporis pontobulbaris contained very high (> 60 fmol/mg wet tissue) and high concentrations of somatostatin binding sites, respectively, while the other relay nuclei contained low to moderate levels of binding. In monoaminergic nuclei, very high and moderate to high concentrations of somatostatin binding sites were measured in the nucleus locus coeruleus and in its dorsal subnucleus, respectively. Moderate densities of sites were detected in the ventral subnucleus of the nucleus locus coeruleus and in the different parts of the raphe. In the white matter, low levels of binding were measured in the inferior cerebellar peduncle, the lateral and median lemnisci and the tractus solitarius. Conversely, moderate to high concentrations of somatostatin binding sites were measured in the median and superior cerebellar peduncles. The pyramis contained a very high density of recognition sites. A marked heterogeneity in the density of binding sites was observed within a few structures particularly in the medial accessory olivary of nucleus and the medial longitudinal fasciculus. Selective ligands were used to determine the pharmacological profile of the [Tyr11]somatostatin-14 binding sites in various brainstem regions. In the dorsal cochlear nucleus and the pyramis, all somatostatin binding sites belonged to the SSA subtype. Conversely, in the lateral paragigantocellular nucleus, all somatostatin binding sites belonged to the SSB subtype. The other regions studied contained various proportions of SSA and SSB subtypes. In conclusion, the present study shows that high concentrations of somatostatin receptors are present in many regions of the human fetus brainstem. These data support the concept that somatostatin could be involved in the maturation of brain structures.

Metabolic fate of an oral tracer dose of [13C]docosahexaenoic acid triglycerides in the rat.

The appearance of 13C in rat lipoprotein, blood cells, and brain lipids was followed as a function of time after the ingestion of triglycerides (TG) containing [13C]22:6n-3. The time course of 13C abundance in 22:6n-3 of various lipid pools, measured by gas chromatography combustion-isotope mass spectrometry, established precursor-product relationships within lipids. The [13C]22:6n-3 was rapidly incorporated into very low density lipoprotein-chylomicron-TG and unesterified fatty acids bound to albumin, with a concomitant maximal appearance at 3 h and further decline. Lysophosphatidylcholines (lysoPC) bound to albumin were also enriched in [13C]22:6n-3, and their labeling appeared to be mainly due to hepatic secretion at the earliest time points. From 12 h postingestion, the synthesis of [13C]22:6n-3-lysoPC was twice as high as that of unesterified [13C]22:6n-3, making lysoPC a potential source of 22:6n-3 supply for tissues. The labeling of platelets, red blood cells, and brain phospholipids presented different kinetics, presumably involving the two lipid forms of [13C]22:6n-3 bound to albumin, to different extents. We conclude that [13C]22:6n-3 esterified in TG is rapidly redistributed within blood lipoproteins and the albumin fraction and that its incorporation in lipid species bound to albumin influences its uptake by target tissues.

In vivo compartmental metabolism of 13C-docosahexaenoic acid, studied by gas chromatography-combustion isotope ratio mass spectrometry.

The exchange of docosahexaenoic acid (22:6n-3) within lipid pools in rat and human has been followed as a function of time after the ingestion of triglycerides (TG) containing 22:6n-3 labeled with 13C(13C 22:6n-3). The 13C abundance in the fatty acid was measured by gas-chromatography-combustion isotope ratio mass spectrometry which allowed the detection of 0.001 atom 13C percent 12C. The 13C 22:6n-3 appearance was rapid in the TG of very low density lipoprotein plus chylomicron fraction, in which the maximal labeling was observed at 3 and 2 h after ingestion in rat and human, respectively. Concomitant with the TG utilization of this fraction by lipoprotein lipase from tissues, unesterified 13C 22:6n-3 appeared in the plasma albumin. 13C 22:6n-3 bound to albumin was mostly present in unesterified form before 12 h post-ingestion while after that period, lysophosphatidylcholine (lysoPC) bound to albumin carried higher 13C 22:6n-3 concentrations. These lyso-PC were mostly from hepatic origin and might represent a potential source of 22:6n-3 redistribution to tissues. The 13C 22:6n-3 uptake into rat brain PC and phosphatidylethanolamine was still increasing when the concentration of plasma unesterified 13C 22:6n-3 had already dropped to a minimal plateau value and during the period of maximal plasma circulation of 13C 22:6n-3-lysoPC bound to albumin. In contrast, the uptake of 13C 22:6n-3 into blood platelet PC occurred during the phase of important circulation of 13C-22:6n-3 bound to albumin, suggesting the in vivo efficiency of the Lands pathway for this fatty acid. It is concluded that 13C 22:6n-3 esterified in TG is rapidly absorbed and redistributed within plasma lipoproteins and that its redistribution within the two lipid species bound to albumin might influence its uptake by platelets and rat brain.

Biliary tract cryptosporidiosis immunosuppressed rat model.

Rats immunosuppressed by hydrocortisone acetate and a low protein diet were challenged with Cryptosporidium Parvum oocysts and studied on days 10, 35 and 70 post-infection. The biliary tract was found to be a major site of parasite infection. C. parvum was visible in the biliary papillary area in association with a proliferation of highly convoluted tubular glands. The papillary lumen was narrowed, and an upstream dilation with bacterial proliferation was seen. The liver was initially free of lesions, and subsequently exhibited late lesions of cholestasis. Parasites were not found in the pancreatic duct, although pancreatitis was frequently observed. Oocysts were consistently present in the distal portion of the ileum. Both challenged and unchallenged immunosuppressed rats, exhibited widespread focal hepatic infarcts and pyelonephritis. Other organs appeared free of lesions. In addition to the intestine, data identified the biliary tract as a major site of C. parvum infection and as a potential protected reservoir which may sustain a chronic infection.

Determination of manganese in human brain samples.

A method is presented for the determination of manganese (Mn) in human tissue samples (especially brain) by graphite furnace atomic absorption spectrophometry (GFAAS). After complete digestion by a mixture of concentrated nitric acid (HNO3)/concentrated perchloric acid (HClO4) (50:50, v/v), the samples are assayed on a Perkin-Elmer 5100 PC apparatus, equipped with transversal graphite tubes and a Mn-specific hollow cathode lamp. The furnace conditions are as follows (for each step: temperature (degree C)/ramp (s)/duration (s)) dry 120/1/40; char 1200/5/10; atomization 2250/0/4; pyrolysis 2400/1/1. Zeeman correction is employed. The method is linear over the range 0.05 to 5.00 micrograms/g wet tissue, and the limit of detection for Mn is about 0.01 microgram/g wet tissue. This simple and rapid method may be of value for the post-mortem assessment of Mn accumulation in brain structures due to occupational or iatrogenic exposure. An application is presented in which elevated levels of Mn were determined in the brain samples of a 63-year-old female deceased after long-term total parenteral nutrition involving Mn supplementation.

Catastrophic antiphospholipid syndrome with fatal acute course in rheumatoid arthritis.

A 34-year old woman, with a 3 yr history of severe seropositive rheumatoid arthritis (RA) with lupus anticoagulant and anticardiolipin antibodies, developed a massive anterior myocardial infarction and ischemia of the lower extremities, with disseminated intravascular coagulation resulting from extensive tissue damage. Seven days after admission, she died of severe heart failure complicated by ventricular fibrillation. To our knowledge, this is the first documented case of fatal acute antiphospholipid syndrome in RA.

Respiratory tract cryptosporidiosis in immunosuppressed rat is associated with an epithelial metaplasia.

Cryptosporidium parvum is an opportunistic protozoa that chronically infects the digestive tract of immunocompromised hosts. Respiratory cryptosporidiosis, which was reported in AIDS patients, is an uncommon feature of mammalian cryptosporidiosis models. In this study, we document the respiratory lesion; observed in an immunosuppressed rat model of cryptosporidiosis. Twenty rats were immunosuppressed with corticosteroids and low protein diet. They were challenged intratracheally with 10(6) C. parvum sporozoites. Lungs and ileums were examined on D3, D6, D10, D14. On D10 and D14, C. parvum were present in the respiratory tract of all animals in association with the progressive appearance of an immature malpighian metaplasia. On D14, an intestinal infection was also detected in 2/4 animals. The respiratory tract appears to be a fully permissive area for the protozoa in immunosuppressed rats. Introduction of parasites on the respiratory mucosa seems a requisite to induce respiratory cryptosporidiosis. This experimental protocol yields a low mortality rate, and so modelizes late and/or chronic stages of respiratory cryptosporidiosis.

A large pedigree with early-onset Alzheimer's disease: clinical, neuropathologic, and genetic characterization.

We present clinical, neuropsychological, and neuropathologic data on a large pedigree including 34 subjects with early-onset progressive dementia. The mean (+/- SD) age at onset was 46 +/- 3.5 years and the mean age at death 52.6 +/- 5.7 years. Twelve patients were clinically diagnosed as having probable Alzheimer's disease (AD) according to the NINCDS-ADRDA criteria. Neuropsychological evaluation, performed at a moderate stage of the disease, was available in six subjects and showed a classic pattern of cognitive deficit. Myoclonus and extrapyramidal signs were common, and seizures were present in all affected subjects. There were neuropathologic changes typical of AD in two brains. A significant lod score of 5.48 was observed at a recombination fraction of theta = 0.0 with the genetic marker D14S43, thereby establishing that the responsible gene was located on chromosome 14q24.3. These results suggest that epilepsy could represent a particular feature in AD families linked to chromosome 14q.

Quantitative autoradiographic study of somatostatin receptors in the adult human cerebellum.

The evolution of the distribution and density of somatostatin receptors was studied in the human cerebellum during ageing. The brain tissues were collected 3-30 h after death from 20 individuals aged from 28 to 86 years. In vitro autoradiographic experiments were performed on blocks of vermis and of right and left cerebellar hemispheres, using [125I-Tyr0,DTrp8]S14 as a radioligand. In the vermis, the mean concentrations of somatostatin receptors in the molecular layer, the granular layer and the medulla were 140 +/- 9, 150 +/- 22 and 61 +/- 13 fmol/mg proteins, respectively. For each individual, the density of sites in the two lateral lobes was similar. The mean concentrations of somatostatin receptors in the molecular layer, the granular layer and the medulla were 152 +/- 17, 190 +/- 20 and 56 +/- 11 fmol/mg proteins, respectively. The mean level of somatostatin receptors and the type of distribution of the receptors were not correlated to the age of the patients. Different distribution patterns of somatostatin receptors were noted among the patients studied. In the majority of patients (11/20), the density of somatostatin receptors was higher in the granular layer than in the molecular layer. Conversely, in four patients, the density of somatostatin receptors was higher in the molecular layer. The other individuals exhibited similar concentrations of somatostatin receptors in the granular and molecular layers. The present study indicates that the adult human cerebellum contains a high concentration of somatostatin receptors (> 100 fmol/mg proteins) and that the receptor level does not decline during ageing.(ABSTRACT TRUNCATED AT 250 WORDS)

Stable isotope tracer and gas-chromatography combustion isotope ratio mass spectrometry to study the in vivo compartmental metabolism of docosahexaenoic acid.

A gas-chromatography combustion isotope ratio mass spectrometry (GCC-IRMS) method using carbon 13 (13C)-stable isotope to trace n-3 polyunsaturated fatty acids (PUFA) turnover in vivo is presented. Natural 13C abundance of commercial n-3 PUFA was measured from 100 to 300 ng of fatty acids and was -27.58, -27.83, and -28.16 for 22:6n-3, 22:5n-3, and 20:5n-3, expressed as delta 13C /1000 versus Pee Dee Belemnite (PDB), respectively. Precision of delta 13C /1000 values was comparable for the three PUFA and gave relative standard deviations of 0.95-0.97%. Isotope enrichment of 0.0010 at.% could be detected. Triglycerides enriched in [13C]22:6n-3 ([13C]22:6-TG) were synthesized by growing a microalgae on [1-13C]glucose. [13C]22:6n-3 represented 36 wt.% of total triglyceride fatty acids and had an isotope enrichment of 2.0420 at.%, which was the double of natural abundance. The isotope enrichment of 22:6n-3 in lipids from rat lipoproteins and red cells could be followed as a function of time after ingestion of 3 mg [13C]22:6-TG and showed specific patterns according to the lipid compartments. The retroconversion of [13C]22:6n-3 was also detected in HDL phosphatidylcholine by the appearance of [13C]22:5n-3 and [13C]20:5n-3. On the other hand, 22:6n-3 natural 13C abundance in human lipid classes of lipoproteins and blood cells has been measured using 10 ml plasma, even for the more limiting lipid compartments in terms of 22:6n-3 dose size.(ABSTRACT TRUNCATED AT 250 WORDS)

Localization and solubilization of hyaluronan and of the hyaluronan-binding protein hyaluronectin in human normal and arteriosclerotic arterial walls.

Hyaluronectin (HN), a hyaluronan (hyaluronic acid, HA)-binding glycoprotein isolated from human brain, was studied in normal and atherosclerotic human arteries. It can be detected and assayed in tissue samples by immunohistochemistry. In addition, its high and specific affinity for HA makes it possible to develop specific histological localization of HA using HN as a probe. We tested the presence of HN and HA in human carotid artery samples from adults and newborns. In atheroma-free arterial samples HN was found in the intima, between smooth muscle cells and in the adventitial extracellular matrix. In atherosclerotic lesions, HN was strongly expressed in the diffuse thickened intima and surrounding extracellular microcrystalline calcium deposits, and very little in the lipid core. HA was found in the same locations. The similar localizations of HN and HA shown by immunohistology and demonstration of HN-HA complexes by high pressure liquid chromatography (HPLC) suggest that they are associated in vivo.

Phospholipid molecular species from human placenta lipids.

The phospholipid molecular species from a large-scale preparation of human placenta lipids were analyzed. The major placental phospholipids were choline glycerophospholipids (CPL) (53.2 wt%), sphingomyelin (21.7 wt%) and ethanolamine glycerophospholipids (EPL) (14.6 wt%). 1,2-Diacyl-glycerophosphocholine was the most abundant subclass of CPL (91.7 mol%), while EPL contained 1,2-diacyl (54.6 mol%) and 1-alk-1'-enyl-2-acyl (43.8 mol%) subclasses. The level of polyunsaturated fatty acids (PUFA) in total phospholipids was remarkably constant (38.4-39.9 mol%) within all placental batches tested. The long-chain PUFA, mainly 20:4n-6 and 22:6n-3 of the n-6 and n-3 series, respectively, were found in high proportion in all phospholipid classes, especially in EPL (46.7 mol%) and in inositol glycerophospholipids (IPL) (39.9 mol%). CPL and serine glycerophospholipids were much richer in 18:1n-9 and 18:2n-6. High levels of molecular species with arachidonic acid in the sn-2 position were found particularly in 1-alk-1'-enyl-2-acyl-glycerophosphoethanolamine (with 24.0 mol% 16:0 and 22.0 mol% 18:0 in sn-1 position) and in 1,2-diacyl glycerophosphoinositol with 42.6 mol% 18:0 in sn-1 position. EPL subclasses were rich in 22:6n-3, which occurs mainly as 16:0/22:6n-3 (11.7 mol%) in the plasmalogen form and as 18:0/22:6n-3, 16:0/22:6n-3 and 18:1/22:6n-3 in the diacyl forms. Based on their availability and composition, placental phospholipids could be of interest, for example, for supplementing artificial milk preparations with n-3 and n-6 long-chain PUFA for newborn infants with insufficiently developed 18:2n-6 and 18:3n-3 desaturation/elongation.

Hyaluronan and hyaluronectin in the extracellular matrix of human brain tumour stroma.

Hyaluronan (HA) and the hyaluronan-binding glycoprotein hyaluronectin (HN) were measured in 23 gliomas and 8 meningiomas and their location was revisited in 35 tumours. A clear-cut difference was found in the HN/HA ratio values of glioblastomas (below 0.5) and that of astrocytomas (above 0.5 P < 0.001). Besides their location in the intercellular part of gliomas, HA and HN displayed a perivascular location in 1/3 astrocytomas, 17/24 glioblastomas, and 3/7 meningiomas, suggesting they could be produced also by the vascular stroma of tumours and that they would characterise the neoangiogenesis. All cultivated glioma cells tested produced HA in vitro, whereas only 1/11 cell lines produced HN, at a low level. The results obtained suggest that glioma HA and HN are produced by both cancer cells and vascular stroma cells, which contribute to the edification of the extracellular matrix. In meningiomas only the stroma would be responsible for HA and HN production.