Trilaminar Structures Research Articles

Aramid nanofiber based Ag/Fe3O4-CNT/rGO hybrid membrane for high-performance electromagnetic interference shielding

With the increase of modern integrated electronic and telecommunication systems, high-performance electromagnetic interference (EMI) shielding materials with flexibility, outstanding thermal conductive properties and superior EMI shielding performances are designed to solve the problems of electromagnetic radiation and heat accumulation. Herein, flexible asymmetric trilaminar architecture film with good mechanical properties is prepared via the facile three-step vacuum-assisted filtration (VAF) followed by hot-pressing approach, which is composed of silver-plated aramid nanofibers (ANF-Ag), ANF-Fe3O4&CNT (ANF-FC) and ANF-reduced graphene oxide (ANF-rGO) layers. The conductive ANF-Ag and ANF-rGO layers acted as the EMI shielding, thermal conductive layers, and supporting substrate layers. The magnetic ANF-FC layer played the important role in synergistically enhancing the EMI shielding performance. The resultant flexible and asymmetric trilaminar hybrid membrane with a thickness of 112 µm exhibited maximum thermal conductivity of 8.5 W m−1 K−1 and EMI SE of 67.5 dB, but also maintained a high tensile strength of 75.5 MPa and superb electrical conductivity of 2.46 × 106 S/m. This asymmetric trilaminar structures film holds great promise to addresses issues of electromagnetic radiation and heat accumulation for personal smart electronic devices, wearable electronics, electronic telecommunication systems.

Abstract P1178: APOE-NOTCH Axis Governs Elastogenesis During Human Cardiac Valve Remodeling

Background: Valve remodeling is a complex process involving extracellular matrix organization, development of trilaminar structures, and physical elongation of valve leaflets. However, the cellular and molecular mechanisms regulating valve remodeling and their roles in congenital valve disorders remain poorly understood. Methods: Semilunar valves and atrioventricular valves from healthy and age-matched human fetal hearts with pulmonary stenosis (PS) were collected. Single-Cell RNA-sequencing (scRNA-seq) was performed to determine the transcriptomic landscape of multiple valvular cell subtypes in valve remodeling and disease. Results: scRNA-seq analysis of healthy human fetal valves identified a novel APOE+ elastin-producing valve interstitial cell (Elastin-VIC) subtype spatially located underneath VECs in the direction of unidirectional flow. Knockdown of APOE in fetal VICs resulted in significant elastogenesis defects. In pulmonary valve with PS, we observed decreased expression of APOE and other genes regulating elastogenesis such as EMILIN1 and LOXL1 , as well as elastin fragmentation. Cell-cell interaction analysis revealed that JAG1 from unidirectional VECs activates NOTCH signaling in Elastin-VICs through NOTCH3. In vitro Jag1 treatment in VICs increased the expression of elastogenesis-related genes and enhanced contractile functions with related gene expression. This was accompanied by activation of NOTCH signaling and elastogenesis observed in VICs co-cultured with VECs in the presence of unidirectional flow. Notably, we found that the JAG1-NOTCH3 signaling pair was drastically reduced in the PS valves. Lastly, we demonstrated that APOE is indispensable for JAG1-induced NOTCH activation in VICs, reinforcing the presence of a synergistic intrinsic and external regulatory network involving APOE and NOTCH signaling that is responsible for regulating elastogenesis during human valve remodeling. Conclusion: scRNA-seq analysis of human fetal valves identified a novel Elastin-VIC subpopulation, and revealed mechanism of APOE and NOTCH signaling mediated elastogenesis during valve remodeling, which provided opportunity to understand pathogenesis of elastic malformation within congenital valve disease.

3 KeV H<sub>2</sub><sup>+</sup> Irradiation to Li/Pd/Cu Trilaminar Neutron Production Target for BNCT

For the purpose of avoiding the radiation blistering of the lithium target for neutron production in BNCT (Boron Neutron Capture Therapy) device, trilaminar Li target, of which palladium thin layer was inserted between cupper substrate and Li layer, was newly designed. The Li/Pd/ Cu trilaminar structures of the synthesized target were characterized under 3keV H2 + irradiation by XPS and XAFS technique, which provides structural/electronic properties of solids, and information about the local structure, such as the nature and number of surrounding atoms and inter-atomic distances. The following conclusions were derived; Pd­Cu physical bonding was produced between the Pd and Cu interface by electro-less plating Pd deposition on a high purity Cu plate. From the XAFS observation of white line of Pd, the Pd L3 edge jump was found after H2 + irradiation, this fact indicates increase of hole density in Pd 4d-band. 0.9eV chemical shift was also observed in Pd L3 white line for monolayer and 1µm Pd/Cu samples, which will affect the quality of the Li/Pd/Cu target due to the formation of PdHx in palladium insert layer.

Cell wall ultrastructures of the Proterozoic acritarch Leiosphaeridia asperata and their implications for biological affinity

Abundant sphaeroidal acritarch Leiosphaeridia asperata, with vesicle size ranging from 13 to 360 μm, occurred in the Proterozoic Liulaobei Formation shales in Huainan, Anhui Province. TEM/SEM studies of these sphaeroidal acritarchs have revealed complex ultrastructures, including ridges, bands, and possible trilaminar structures (TLS). Ridges, spaced ∼1 μm apart, are distributed regularly on the vesicle internal surface of one specimen. Some specimens have alternating electron-dense and electron-tenuous bands that are perpendicular to vesicle walls. Some specimens have trilaminar structures (TLS), while a few others have both bands and TLS. These wall ultrastructures provide evidence that the Liulaobei leiosphaerids are of green microalgae. The variation in wall ultrastructures may represent various stages in a life cycle or developmental phases in the cyst formation analogous to some modern chlorophyceaen microalgae.

Targeting of Tsc13p to Nucleus–Vacuole Junctions: A Role for Very-Long-Chain Fatty Acids in the Biogenesis of Microautophagic Vesicles

TSC13 is required for the biosynthesis of very-long-chain fatty acids (VLCFAs) in yeast. Tsc13p is a polytopic endoplasmic reticulum (ER) membrane protein that accumulates at nucleus-vacuole (NV) junctions, which are formed through Velcro-like interactions between Nvj1p in the perinuclear ER and Vac8p on the vacuole membrane. NV junctions mediate piecemeal microautophagy of the nucleus (PMN), during which bleb-like portions of the nucleus are extruded into invaginations of the vacuole membrane and degraded in the vacuole lumen. We report that Tsc13p is sequestered into NV junctions from the peripheral ER through Vac8p-independent interactions with Nvj1p. During nutrient limitation, Tsc13p is incorporated into PMN vesicles in an Nvj1p-dependent manner. The lumenal diameters of PMN blebs and vesicles are significantly reduced in tsc13-1 and tsc13-1 elo3-Delta mutant cells. PMN structures are also smaller in cells treated with cerulenin, an inhibitor of de novo fatty acid synthesis and elongation. The targeting of Tsc13p-GFP into NV junctions is perturbed by cerulenin, suggesting that its binding to Nvj1p depends on the availability of fatty acid substrates. These results indicate that Nvj1p retains and compartmentalizes Tsc13p at NV junctions and that VLCFAs contribute to the normal biogenesis of trilaminar PMN structures in yeast.

The MADS-box transcription factor SrfA is required for actin cytoskeleton organization and spore coat stability during Dictyostelium sporulation

The MADS-box transcription factor SrfA is involved in spore differentiation in Dictyostelium [Development 125 (1998) 3801]. Mutant spores show an altered morphology and loss of viability. A detailed structural analysis of mutant spores has been performed to gain insight into the specific aspects of spore differentiation in which SrfA is involved. Two main structural defects have been observed. One is the formation of high order actin structures, the so-called actin rods. SrfA mutant spores showed the initial stages of rod formation but no mature rods were found in older spores either in the nucleus or the cytoplasm. Moreover, phosphorylation of actin, that is believed to stabilize the actin rods, is strongly reduced in the mutant. The other defect observed was the formation of the spore coat. Young srfA − spores show basically normal trilaminar coat structures suggesting that release of prespore vesicles and basic assembly of the coat takes place in the absence of SrfA. However, the outer layer gets wavier as the spore ages and suffers a progressive degradation suggesting a late defect in the stability of the spore coat. Taken together, these results suggest that SrfA is involved in late events of spore maturation necessary for spore stability.

Olfactory recognition memory

Olfactory recognition which occurs in the context pregnancy block by male pheromones is acquired with one-trial learning contingent on mating. A memory trace is established in the accessory bulb (AOB) and is represented by a gain in Gaba-ergic feedback inhibition of granule cells on excitatory glutaminergic mitral cells. This occurs in the sub-population of mitral cells that specifically respond to an individual male's pheromones, and is dependent on noradrenaline release at mating. Although relatively simple, the AOB has both structural and functional similarities with other trilaminar neural structures involved in learning, which suggests some evolutionary conservation of mechanisms subserving memory.

CENP-C is required for maintaining proper kinetochore size and for a timely transition to anaphase.

The human autoantigen CENP-C has been demonstrated by immunoelectron microscopy to be a component of the inner kinetochore plate. Here we have used antibodies raised against various portions of CENP-C to probe its function in mitosis. We show that nuclear microinjection of anti-CENP-C antibodies during interphase causes a transient arrest at the following metaphase. Injection of the same antibodies after the initiation of prophase, however, does not disrupt mitosis. Correspondingly, indirect immunofluorescence using affinity-purified human anti-CENP-C antibodies reveals that levels of CENP-C staining are reduced at centromeres in cells that were injected during interphase, but appear unaffected in cells which were injected during mitosis. Thus, we suggest that the injected antibodies cause metaphase arrest by reducing the amount of CENP-C at centromeres. Examination of kinetochores in metaphase-arrested cells by electron microscopy reveals that the number of trilaminar structures is reduced. More surprisingly, the few remaining kinetochores in these cells retain a normal trilaminar morphology but are significantly reduced in diameter. In cells arrested for extended periods, these small kinetochores become disrupted and apparently no longer bind microtubules. These observations are consistent with an involvement of CENP-C in kinetochore assembly, and suggest that CENP-C plays a critical role in both establishing and/or maintaining proper kinetochore size and stabilizing microtubule attachments. These findings also support the idea that proper assembly of kinetochores may be monitored by the cell cycle checkpoint preceding the transition to anaphase.

Grafts of dissociated cerebellar cells containing Purkinje cell precursors organize into zebrin I defined compartments

A prominent feature of the mammalian cerebellum is its organization into parasagittal compartments. One marker of such compartments is the zebrin I molecule that is expressed by bands of Purkinje cells (PC). In order to understand better the basis for the development of this organization, we have transplanted dissociated rat cerebellar anlage, taken during the period of proliferation of PC precursors, into kainic acid lesioned adult rat cerebellum. As previously observed, the resultant grafts exhibited trilaminar structures reminiscent of the normal cerebellum. In every case, the PC in the resultant grafts were organized into zebrin I+ and - compartments. In one case, most of the grafted PC were integrated into a region of PC deficient host molecular layer that was induced by pretreatment with kainic acid. Clear bands defined by zebrin I reactivity were seen where groups of the grafted PC had entered the host molecular layer. These bands did not correlate in distribution or size with host bands. Hypotheses compatible with these findings that involve specific and non-specific aggregation of PC are discussed.

Polarizing inclusions in some organs of children with congenital peroxisomal diseases (Zellweger's, Refsum's, chondrodysplasia punctata (rhizomelic form), X‐linked adrenoleukodystrophy)

Polarizing material has been reported in the liver of children with infantile Refsum's disease (IRD) and was absent in two patients with the cerebro-hepato-renal syndrome of Zellweger (CHRS). We examined in polarized light 15 liver biopsy and autopsy samples from six other patients with the cerebro-hepato-renal syndrome of Zellweger, two with the rhizomelic form of chondrodysplasia punctata (rCDP) and two with X-linked adrenoleukodystrophy (ALD), all conditions with deficient peroxisomes. Two types of birefringent inclusions were found in CHRS only: the first is transparent in bright field, the second appears as brown granules or rods, similar to lipofuscins. As in IRD large PAS-positive macrophage-like cells contain the transparent type. Electron microscopical investigation of these cells shows trilaminar structures within membrane-bound organelles. The two types were also seen in kidney and brown adipose tissue, the first type in pancreas, the second type in adrenal gland; no such was observed in myocardium or in thyroid gland (CHRS). No birefringent inclusions were present in rCDP and ALD. The nature of the inclusions is still unclear. An accumulation of the transparent polarizing material with increasing age of the patients is most likely.

Ultrastructural, histochemical, and freeze‐fracture evaluation of multilamellated structures in human pulmonary alveolar proteinosis

Ultrastructural, histochemical, and freeze-fracture studies of material recovered by bronchoalveolar lavage from patients with pulmonary alveolar proteinosis revealed four types (A, B, C, and D) of multilamellated structures (MS). Type A, the major component, consisted of concentric, trilaminar structures which were composed of two electron-dense layers and a central lucent layer (5.7-7.5 nm in overall width) alternating with wider (25-30 nm) electron-lucent intervening layers. Type B MS were formed by concentric lamellae with a 5-5.3-nm periodicity. Type C MS were composed of wavy, electron-dense lamellae with a 4-4.5-nm periodicity. Type D MS were conglomerated masses of intricately arranged double or triple electron-dense layers (7.5-13.5 nm wide) alternating with wider (30-40-nm) electron-lucent layers. The electron-dense lamellae of type A, type C, and type D MS were stained with ruthenium red, the Thiéry method, and concanavalin A, indicating the presence of carbohydrate components. Freeze-fracture studies revealed smooth inner and outer surfaces in type A MS, with the fracture planes passing through the central parts of the trilaminar structures; the intervening layers contained 10-nm particles, which probably are proteins. Type B MS had smooth surfaces, and type C MS had slightly particulate surfaces; while type D MS showed tubular or polygonal structures, 350 nm wide, with rows of particles 7-8 nm in diameter. It is concluded that type A and type D MS contain proteins and carbohydrates, probably in the form of glycoproteins, as well as phospholipids, and are related to tubular myelin. Type B and type C MS are considered to contain mainly phospholipids; type C MS are also considered to contain carbohydrates and to be related to lamellar bodies of type II alveolar epithelial cells.

Dysmorphic syndrome with phytanic acid oxidase deficiency, abnormal very long chain fatty acids, and pipecolic acidemia: Studies in four children

We describe a relatively new syndrome in four children with characteristic facial dysmorphism, sensorineural hearing loss, severe visual impairment with retinitis pigmentosa, hypotonia, hepatomegaly, and severe developmental delay. Two patients had intracranial hemorrhage secondary to a vitamin K-responsive clotting defect; both had steatorrhea. Liver biopsy specimens in two children showed an accentuated lobular architecture with prominent fibrous bands in the portal area. In one, the ultrastructure showed accumulation of abnormal substances and occasional trilaminar structures in hepatocytes and other cells. All four patients had elevated serum phytanic acid concentrations (0.3 to 2.7 mg/dl, normal less than 0.2 mg/dl) and deficient fibroblast phytanic acid oxidase activity (0.1 to 6.7 pmol/mg protein/hr, normal 23 to 87 pmol/mg protein/hr). Serum pipecolic acid was 7 to 55 times normal, and the ratio of C26/C22 very long chain fatty acids was increased (0.10 to 0.22; normal less than 0.03). This characteristic syndrome has been described in several children and called infantile Refsum disease or phytanic acid storage disease. Its relationship to neonatal adrenoleukodystrophy, hyperpipecolic acidemia, and Zellweger syndrome is discussed.

Choroideremia: A Clinical, Electron Microscopic, and Biochemical Report

An asymptomatic 19-year-old male with choroideremia had diffuse loss of retinal pigment epithelium (RPE) and choroid except for the periphery and macula. Fluorescein angiography of the arteriovenous phase showed absence of retinal pigment epithelium and exaggerated visualization of choroidal vessels in involved areas. The mother was a typical carrier with pigment stippling of the midperipheral retina. Histopathologic examination of affected areas of one eye showed marked degeneration of the outer and midretina with loss of retinal pigment epithelium and Bruch's membrane, absence of choriocapillaris, chorioretinal adhesions and gliosis. Atrophy of inner and mid-choroid was also observed. Pigmented macrophage-like cells had migrated into the outer and midretinal layers. Electron microscopy disclosed macrophage-like cells with trilaminar structures and photoreceptor phagosomes in the RPE and outer retina. Remnants of photoreceptor outer segments were adherent to the plasma membranes of the macrophage-like cells. Biochemical analysis of retinal tissue samples for interphotoreceptor retinoid-binding protein (IRBP) showed marked reduction in the 146K bands in the equator and posterior pole in the patient compared to controls. Cyclic nucleotide content was altered in the retinal equator. Cyclic AMP was several-fold higher in the RPE-choroid complex of the affected eye than in the control

Clinical, biochemical, serological, histological and ultrastructural features of liver disease in drug abusers.

Heroin abusers are frequently found to have abnormal liver function tests and hepatic histology. Hepatitis viruses A, B, and NANB, other drugs or drug contaminants and excessive alcohol consumption are factors thought to contribute. One hundred and sixteen heroin abusers attending a London treatment centre were studied. Sixty two (53%) had a raised aspartate transaminase. This was not explained by current infection with hepatitis A and B, cytomegalo or Epstein-Barr viruses, excessive alcohol consumption (greater than 80 g/day) or concomitant drug taking. Abnormal liver function tests were as frequent in those with markers of current or past HBV infection as those without and there was evidence that both HBV infection and the cause of the abnormal liver function tests were acquired in the first few years of intravenous drug abuse. Liver biopsies from eight patients showed chronic hepatitis with a mild lobular and portal inflammatory infiltrate, fatty change and prominent sinusoidal cells. Electron microscopy showed cytoplasmic trilaminar tubular structures and dense fused membranes in dilated endoplasmic reticulum. These clinical, biochemical, serological, and histological features would suggest a major role for NANB virus infection in the aetiology of hepatitis in heroin abusers.

SPORE WALL DEVELOPMENT IN ANDREAEA (MUSCI: ANDREAEOPSIDA)

The spore wall of Andreaea rothii (Andreaeopsida) is unique among mosses studied by transmission electron microscopy. The exine of other mosses is typically initiated on trilaminar structures of near unit membrane dimensions just outside the plasma membrane. The exine of Andreaea is initiated in the absence of such structures as discrete globules within the coarsely fibrillar network of the sporocyte wall. The sequence of wall layer development, nevertheless, is essentially like that of other mosses. The intine is deposited within the exine and the perine accumulates on the surface of the exine during the latter stages of spore maturation. The mature spore is weakly trilete and inaperturate. The wall consists of three layers, the inner intine, the spongy exine consisting of loosely compacted irregular globules of sporopollenin, and an outer layer of perine. The perine differs ultrastructurally from the exine only in its greater degree of electron opacity. This ultrastructural evidence of departure from the fundamental pattern of exine development in mosses supports the taxonomic isolation of Andreaea from mosses of the Sphagnopsida and Bryopsida.

Morphology and distribution of cytoplasmic inclusions in adrenoleukodystrophy

We report some additional observations on the pathognomonic cytoplasmic inclusions in a typical case of adrenoleukodystrophy (ALD). Study of the linear inclusions by means of tilt-stage electron microscopy indicated that they represent trilaminar sheet-like structures distinct from materials seen in various other storage disorders. This study emphasizes that the inclusions in the adrenal and testicular parenchymal cells morphologically differ from those in the brain macrophages. In the latter they occur as membrane-bound discrete structures while in the parenchymal cells they are always seen lying free in the cytoplasm and associated with cleft-like spaces. This morphologic variation of the inclusions is noteworthy and probably reflects a biochemical difference in the storage materials in these two most severely affected organs. In addition, this study demonstrates the presence of linear inclusions within macrophages in otherwise normal-appearing liver, spleen, thymus and also in the renal tubular cells. These findings suggest that the abnormal materials containing very long chain fatty acids enter the blood stream and become sequestered in the reticuloendothelial system and possibly are also excreted in the urine. Detection of these abnormal fatty acids in blood and urine may simplify diagnosis of ALD.

Lysosomal degradation of cell organelles: IV. Heterophagocytosis and acute inflammation in liver after intravenous injection of isolated liver-cell plasma membranes

Isolated liver-cell plasma membranes were injected intravenously into a series of highly inbred rats. The uptake and digestion by Kupffer cells were followed by ultrastructural analysis in order to evaluate the capacity of lysosomes to degrade cellular membranes. By 1 to 5 min following administration, clusters of plasma membranes appeared in the sinusoidal lumens. Invaginations of the Kupffer-cell surfaces in combination with flap-like processes embraced the aggregates and formed endocytic vacuoles. Fibrinous deposits and platelet accumulation were sometimes observed at the surface of the Kupffer cells. At later time points (10 min to 2 hr) an increased number of plasma-membrane derivatives with trilaminar structures still recognizable was observed in large digestive vacuoles. In some focal areas, an acute inflammatory response was noted in the sinusoids often surrounding clusters of fibrin deposits, trapped erythrocytes, and aggregates of plasma membranes and platelets. At 8 hr there was a clearance from some digestive vacuoles of identifiable membranes with the appearance of dense homogeneous material; plasma membranes were still present in the sinusoids together with degranulating and degenerating leukocytes also phagocytizing plasma membranes. By 24 hr most of the inflammatory response had subsided. Many Kupffer cells resembled those in control animals although the digestive vacuoles or residual bodies contained numerous lipid-like droplets presumed to be remnants of membrane lipid digestion. By 2–5 days the Kupffer cells gradually became indistinguishable from the controls and the micropinocytosis vermiformis reappeared. It is concluded that plasma membranes after being phagocytized are digested within lysosomes. In contrast to mitochondria and microsomes ( Glaumann et al., 1975a b; Glaumann and Trump, 1975), intravenous injections of plasma membranes gave rise to focally occurring thrombi which were surrounded by an acute transient inflammatory response.

The Effect of Viewing Angle on the Appearance of Trilaminar Structures of Desmosomes

Examination of desmosomes in the spinous region of the epidermis of human skin reveals that the trilaminar structure, usually associated with desmosomes, is not always observed. Desmosomes were examined utilizing serial sectioning and tilting techniques to determine if the trilaminar structure is consistant throughout the desmosome. Concomitantly, information concerning the size and shape of the spinous layer desmosomes was obtained from examination of serial sections that completely transversed many desmosomes.Figures 1 and 2 are from a serial section series and demonstrate that the trilaminar structure of desmosomes (Dl and D2) can be observed in one section (figure 1) and not observed in an adjacent section (figure 2). Figure 3 thru Figure 6 are micrographs of the same section seen in Figure 2. These micrographs show the effect on the appearance of desmosomes Dl and D2 when they have been tilted about their longitudinal axes 5, 10, 20, and 30 degrees, respectively.

Characterization of endotoxin from Fusobacterium necrophorun.

Endotoxic lipopolysachharide (LPS) was obtained from phenol-water extraction of cell walls prepared from mass-cultivated Fusobacterium necrophorum. The LPS was relatively free of nucleic acids and low in protein, and constituted about 4% of the cell walls. Upon acid hydrolysis, some of the components detected were hexosamines (7.0%), neutral and reducing sugars (50.5%), heptose (6.4%), 2-keto-3-deoxyoctonate (0.8%), lipid A (21.0%), and phosphorus (1.7%). Under electron microscopy the LPS appeared mainly as ribbon-like trilaminar structures, and upon chemical treatment it displayed a behavior resembling that reported in certain enterobacterial LPS. The LPS was lethal to mice, 11-day-old chicken embryos, and rabbits. Endotoxicity in mice was enhanced at least 1,380-fold by the addition of 12.5 mug of actinomycin D. Induced tolerance to lethal effect of the endotoxin and rapidly acquired resistance to infection by F. necrophrum viable cells were also demonstrated in mice. The endotoxin produced both localized and generalized Shwartzman reactions as well as biphasic pyrogenic responses in rabbits. These results firmly establish the presence of a classical endotoxin in F. necrophorum, thus providing strong support to our recent suggestion that cell wall-associated components may contribute significantly to the pathogenicity of F. necrophorum.

The Ultrastructure of Plasma Lipoproteins in Lecithin: Cholesterol Acyltransferase Deficiency

The major plasma lipoprotein classes from patients with familial LCAT deficiency showed morphological abnormalities. Very low density lipoproteins (VLDL) contained particles with surface irregularities as well as sheet-like trilaminar structures which resembled phospholipid bilayers. Three types of particles were seen in the low density (LDL) region, large flattened structures approximately 1, 000A in size, intermediate particles 400–600A in diameter, and normal 200–250A particles. The high density lipoproteins (HDL) were characterized by discoidal particles 40A thick and 150–200A in diameter; these particles formed rouleaux. Abnormal HDL particles could be normalized by incubation of whole LCAT-deficient plasma (or HDL fraction) with LCAT; resulting structures resembled normal HDL (90–110A spheres). In severe liver disease with apparent biliary obstruction the structure of plasma lipoproteins often resembled those of familial LCAT deficiency. Rouleaux, consisting of disc-shaped particles, were in the HDL fraction, and these structures were also normalized by incubation with LCAT. Reassembly studies with apolipoproteins plus phospholipid suggested that the discs represent a bilayer structure stabilized by protein. Cholesteryl ester incorporated into the protein-lipid complex produced spherical particles.