Journal articles: 'Lamines de type A'

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Zinn-Justin, Sophie. "Maladies génétiques et lamines de type A : apport de la biologie structurale." médecine/sciences 18, no. 11 (November 2002): 1054–56. http://dx.doi.org/10.1051/medsci/200218111054.

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Zhang, Xue Yi, Guang Ping Zou, and Li Hong Yang. "Mechanical Properties and Damage Mechanism of Glass Fiber Composite Laminates in Compression." Key Engineering Materials 417-418 (October 2009): 609–12. http://dx.doi.org/10.4028/www.scientific.net/kem.417-418.609.

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Application of composite laminates was very wide in aerospace engineering, civil engineering, wind energy, auto industry, etc. Low cost glass fiber textile was often applied into composite laminates by many composites companies. It is of import that investigation of mechanical properties and damage mechanism of this composites laminates. Two types of composite laminates were studied in this paper. One type of composite laminates was made of glass fiber biaxial cloth. The other was made of glass fiber composite felt. Each type composite laminates has different direction aligned. Many specimen were tested in compression with universal testing materials machine model INSTRON 5500R. Strength of composite laminates and stress-strain diagram was obtained in these experiments. Effect of fiber different orientation on compression strength of laminates was found. Shear stresses between two laminas were calculated. Fracture mechanism of composites laminates was analyzed by macro-method. Fractography of laminates was applied into analysis of mechanism. SEM photo was acquired and observed in detail. The result is that strength and failure mechanism of different types composite laminates varied with fiber orientation and different textiles.

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Genty, Dominique, Andy Baker, and William Barnes. "Comparaison entre les lamines luminescentes et les lamines visibles annuelles de stalagmites." Comptes Rendus de l'Académie des Sciences - Series IIA - Earth and Planetary Science 325, no. 3 (August 1997): 193–200. http://dx.doi.org/10.1016/s1251-8050(97)88288-2.

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Dionne*, Jean-Claude. "Événements holocènes mis en évidence dans une coupe de la terrasse Mitis à l’embouchure de la rivière Fouquette, sur la rive sud du moyen estuaire du Saint-Laurent." Géographie physique et Quaternaire 57, no. 2-3 (September 22, 2005): 241–47. http://dx.doi.org/10.7202/011317ar.

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Résumé Près de l’embouchure de la rivière Fouquette, une coupe d’environ 6 m de hauteur comprend trois unités lithostratigraphiques. Celle à la base (entre 3 et 6 m) est de type rythmique. Elle est composée de couches d’argile gris pâle, plastique et calcaire, et de lamines de sable interstratifiées. Le faciès de cette unité s’apparente à celui des dépôts tidaux de milieu estuarien relativement peu profond (10-15 m) correspondant en l’occurrence à un large chenal empruntant une dépression entre deux crêtes rocheuses appalachiennes. Des débris organiques ligneux récoltés à divers niveaux ont donné des âges au 14C compris entre 8,7 et 10,6 ka BP, ce qui correspond à une mise en place vers la fin de l’épisode de la Mer de Goldthwait, sur la rive sud de l’estuaire du Saint-Laurent. De 2 m d’épaisseur, l’unité 2 est composée de lits minces de limon et de sable fin gris pâle mis en place dans un milieu infratidal à intertidal inférieur. Elle n’a pas été datée. En surface, l’unité 3, d’environ 100 cm d’épaisseur, est sableuse. Elle a probablement été mise en place lors de l’épisode de Mitis dont l’âge moyen est de 2 ka BP. La coupe de la rivière Fouquette révèle une fois de plus que la nature de la terrasse de 6 m (terrasse Mitis) est parfois complexe ; elle peut être formée de dépôts variés mis en place antérieurement à l’épisode de Mitis ; elle confirme aussi que le niveau marin relatif était seulement d’une quinzaine de mètres supérieur au niveau actuel vers 9,5 ka BP.

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Hua, Ganlin, Songtao Wu, Jinyou Zhang, Rongchang Liu, Modi Guan, Yi Cai, Mengying Li, and Surong Zhang. "Laminar Structure and Reservoir Quality of Shales with High Clay Mineral Content in the Qingshankou Formation, Songliao Basin." Energies 15, no. 17 (August 24, 2022): 6132. http://dx.doi.org/10.3390/en15176132.

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This paper investigates high-maturity organic matter-rich shales with high clay mineral contents in the Qingshankou Formation, in the Gulong Depression of the Songliao Basin, at a sub-millimeter scale, using a new laminar division method based on XRF data. The influence of laminar structure on reservoir quality is examined using a combination of geochemistry, mineralogy, and pore structures. Explanatory models are established. Three types of laminar units are distinguished in the study area based on differences in pore structure. These are clay mineral laminae (UA), clay mineral-Ostracod laminae (UB), and clay mineral-felsic laminae (UC). UA has illite intergranular pores, micro-fractures, and organic pores, with diameters of 0.5~2 μm. UB primarily contains Ostracod shell margin fractures, pyrite intergranular pores, and chlorite intragranular pores. UC contains albite and illite intergranular pores. Nitrogen adsorption tests show that UA has the highest clay content and the best specific pore volume and specific surface area, indicating that clay minerals are the main contributors to the pores in this type of unit. 2D–3D models of different laminae reveal that carbonate cement is widely developed in UB and UC, but dissolution pores are less developed, with the result that the porosity of UA is two to three times greater than that of UB or UC. It appears that intergranular pores and fractures, formed during the transformation of clay minerals during the advanced thermal evolution stage, are the main contributors to storage space and flow channels. Thermal evolution, clay mineral transformation, and carbonate cementation are the key factors causing differences between laminar units. In addition, clay mineral laminae (UA) are the most important laminar units for shale oil enrichment in the study area. This finding is of great significance for accurately predicting the distribution of shale “sweet spots” and guiding shale oil and gas exploration.

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Lilina, Anastasia V., Anastasia A. Chernyatina, Dmytro Guzenko, and Sergei V. Strelkov. "Lateral A11 type tetramerization in lamins." Journal of Structural Biology 209, no. 1 (January 2020): 107404. http://dx.doi.org/10.1016/j.jsb.2019.10.006.

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7

Navarro, Claire L., Yannick Poitelon, and Nicolas Lévy. "Lamines A et syndromes progéroïdes." médecine/sciences 24, no. 10 (October 2008): 833–40. http://dx.doi.org/10.1051/medsci/20082410833.

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8

Steen, Rikke L., and Philippe Collas. "Mistargeting of B-Type Lamins at the End of Mitosis." Journal of Cell Biology 153, no. 3 (April 30, 2001): 621–26. http://dx.doi.org/10.1083/jcb.153.3.621.

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We previously showed that targeting of protein phosphatase 1 (PP1) to the nuclear envelope (NE) by the A-kinase anchoring protein, AKAP149, correlates with nuclear assembly of B-type lamins in vitro. We demonstrate here that failure of AKAP149-mediated assembly of B-type lamins into the nuclear lamina at the end of mitosis is followed by apoptosis, and induces expression of the gene encoding A-type lamins in cells that normally do not express lamins A/C. In HeLa cells, inhibition of PP1 association with the NE mediated by a peptide containing the PP1-binding domain of AKAP149 results in failure of B-type lamins to assemble, and in their rapid caspase-dependent proteolysis. However, assembly of lamins A/C is not affected. Nonetheless, apoptosis follows within hours of nuclear reformation after mitosis. In lymphoid KE37 cells, which do not express lamins A/C, inhibition of B-type lamin assembly triggers rapid synthesis and nuclear assembly of both lamins A and C before apoptosis takes place. The results indicate that nuclear assembly of B-type lamins is essential for cell survival. They also suggest that mistargeting of B-type lamins at the end of mitosis elicits a tentative rescue process to assemble a nuclear lamina in lymphoid cells that normally do not express lamins A/C.

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Hanif, Mubashir, Ylva Rosengardten, Hanna Sagelius, Björn Rozell, and Maria Eriksson. "Differential Expression of A-Type and B-Type Lamins during Hair Cycling." PLoS ONE 4, no. 1 (January 5, 2009): e4114. http://dx.doi.org/10.1371/journal.pone.0004114.

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Hutchison, Chris J., and Howard J. Worman. "A-type lamins: Guardians of the soma?" Nature Cell Biology 6, no. 11 (November 2004): 1062–67. http://dx.doi.org/10.1038/ncb1104-1062.

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11

Hutchison, C. J. "B-type lamins in health and disease." Seminars in Cell & Developmental Biology 29 (May 2014): 158–63. http://dx.doi.org/10.1016/j.semcdb.2013.12.012.

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Peter, M., and E. A. Nigg. "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells." Journal of Cell Science 100, no. 3 (November 1, 1991): 589–98. http://dx.doi.org/10.1242/jcs.100.3.589.

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The nuclear lamina is an intermediate filament-type network underlying the inner nuclear membrane. It is believed to be important for nuclear envelope integrity and the organization of interphase chromatin. On the basis of biochemical properties and sequence criteria, vertebrate lamin proteins are classified as either A- or B-type. While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. These findings have led to the hypothesis that A-type lamins might play a role in establishing or stabilizing cell-type specific differences in nuclear organization, which in turn might relate to the developmental potential of a cell. To test this hypothesis, we have stably expressed chicken lamin A in undifferentiated murine embryonal carcinoma (P19) cells, and examined the consequences of ectopic lamin A expression for the differentiation state and potential of these cells. Our results demonstrate that the P19 cells, although normally devoid of lamin A, properly incorporate and process chicken lamin A. Moreover, the stably transfected cell lines maintain the properties of undifferentiated cells, demonstrating that expression of lamin A does not directly induce differentiation. Conversely, when exposed to retinoic acid, an inducer of differentiation, lamin A-expressing P19 cells are able to differentiate normally. Taken together, our results suggest that unscheduled expression of A-type lamins is not sufficient to deregulate cell differentiation programs. The implications of these findings for the possible role for lamin A expression during development are discussed.

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Sears, Rhiannon M., and Kyle J. Roux. "Mechanisms of A-Type Lamin Targeting to Nuclear Ruptures Are Disrupted in LMNA- and BANF1-Associated Progerias." Cells 11, no. 5 (March 2, 2022): 865. http://dx.doi.org/10.3390/cells11050865.

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Mutations in the genes LMNA and BANF1 can lead to accelerated aging syndromes called progeria. The protein products of these genes, A-type lamins and BAF, respectively, are nuclear envelope (NE) proteins that interact and participate in various cellular processes, including nuclear envelope rupture and repair. BAF localizes to sites of nuclear rupture and recruits NE-repair machinery, including the LEM-domain proteins, ESCRT-III complex, A-type lamins, and membranes. Here, we show that it is a mobile, nucleoplasmic population of A-type lamins that is rapidly recruited to ruptures in a BAF-dependent manner via BAF’s association with the Ig-like β fold domain of A-type lamins. These initially mobile lamins become progressively stabilized at the site of rupture. Farnesylated prelamin A and lamin B1 fail to localize to nuclear ruptures, unless that farnesylation is inhibited. Progeria-associated LMNA mutations inhibit the recruitment affected A-type lamin to nuclear ruptures, due to either permanent farnesylation or inhibition of BAF binding. A progeria-associated BAF mutant targets to nuclear ruptures but is unable to recruit A-type lamins. Together, these data reveal the mechanisms that determine how lamins respond to nuclear ruptures and how progeric mutations of LMNA and BANF1 impair recruitment of A-type lamins to nuclear ruptures.

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Shi, Luhuai, Xiaoguang Li, and Hua Qian. "Anti-Laminin 332-Type Mucous Membrane Pemphigoid." Biomolecules 12, no. 10 (October 12, 2022): 1461. http://dx.doi.org/10.3390/biom12101461.

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Anti-laminin (LM) 332-type mucous membrane pemphigoid (MMP) is a rare autoimmune bullous disease and was originally discovered as anti-epiligrin cicatricial pemphigoid. Anti-LM332-type MMP has clinical manifestations similar to those of other types of MMP and can only be distinguished through the detection of circulating autoantibodies against LM332. Our group and others have established a number of immunological methods with varying sensitivity and specificity for detection of anti-LM332 autoantibodies; however, none of the established methods has been widely used for clinical diagnosis. There is currently no unified standard treatment, and it is very difficult to completely cure anti-LM332-type MMP. In addition, an increasing body of evidence suggests that there may be a strong correlation between anti-LM332-type MMP and tumors. In this article, we review the current progression of diagnosis and treatment of anti-LM332-type MMP, as well as the possible correlation between anti-LM332-type MMP and tumors.

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Dechat, T., B. Korbei, O. A. Vaughan, S. Vlcek, C. J. Hutchison, and R. Foisner. "Lamina-associated polypeptide 2alpha binds intranuclear A-type lamins." Journal of Cell Science 113, no. 19 (October 1, 2000): 3473–84. http://dx.doi.org/10.1242/jcs.113.19.3473.

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The nucleoskeletal protein lamina-associated polypeptide 2(α) (LAP2*) contains a large, unique C terminus and differs significantly from its alternatively spliced, mostly membrane-integrated isoforms, such as LAP2beta. Unlike lamin B-binding LAP2beta, LAP2alpha was found by confocal immunofluorescence microscopy to colocalize preferentially with A-type lamins in the newly formed nuclei assembled after mitosis. While only a subfraction of lamins A and C (lamin A/C) was associated with the predominantly nuclear LAP2alpha in telophase, the majority of lamin A/C colocalized with LAP2alpha in G(1)-phase nuclei. Furthermore, selective disruption of A-type lamin structures by overexpression of lamin mutants in HeLa cells caused a redistribution of LAP2alpha. Coimmunoprecipitation experiments revealed that a fraction of lamin A/C formed a stable, SDS-resistant complex with LAP2alpha in interphase cells and in postmetaphase cell extracts. Blot overlay binding studies revealed a direct binding of LAP2alpha to exclusively A-type lamins and located the interaction domains to the C-terminal 78 amino acids of LAP2alpha and to residues 319–566 in lamin A/C, which include the C terminus of the rod and the entire tail common to lamin A/C. These findings suggest that LAP2alpha and A-type lamins cooperate in the organization of internal nuclear structures.

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Guo, Yuxuan, and Yixian Zheng. "Lamins position the nuclear pores and centrosomes by modulating dynein." Molecular Biology of the Cell 26, no. 19 (October 2015): 3379–89. http://dx.doi.org/10.1091/mbc.e15-07-0482.

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Lamins, the type V nuclear intermediate filament proteins, are reported to function in both interphase and mitosis. For example, lamin deletion in various cell types can lead to an uneven distribution of the nuclear pore complexes (NPCs) in the interphase nuclear envelope, whereas deletion of B-type lamins results in spindle orientation defects in mitotic neural progenitor cells. How lamins regulate these functions is unknown. Using mouse cells deleted of different combinations or all lamins, we show that lamins are required to prevent the aggregation of NPCs in the nuclear envelope near centrosomes in late G2 and prophase. This asymmetric NPC distribution in the absence of lamins is caused by dynein forces acting on NPCs via the dynein adaptor BICD2. We further show that asymmetric NPC distribution upon lamin depletion disrupts the distribution of BICD2 and p150 dynactin on the nuclear envelope at prophase, which results in inefficient dynein-driven centrosome separation during prophase. Therefore lamins regulate microtubule-based motor forces in vivo to ensure proper NPC distribution in interphase and centrosome separation in the mitotic prophase.

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Moon, Myung-Sang, Min-Keun Yoon, Ki-Tae Kwon, Min-Suk Park, Bong-Keun Park, and Sung-Soo Kim. "POSTERIOR ELEMENT MORPHOLOGY AND DEGENERATIVE LUMBAR SPONDYLOLISTHESIS." Journal of Musculoskeletal Research 18, no. 01 (March 2015): 1550001. http://dx.doi.org/10.1142/s0218957715500013.

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Study design: Retrospective radiographic studies on lumbar facet morphology, and facet and laminar inclination angles. Objectives: To investigate the effect of the facet morphology, facet and laminar inclination angles on development of the segmental instability and spondylolisthesis. Summary of background data: Many previous papers related with the facet shape on pathogenesis of the degenerative instability and spondylolisthesis were published. Most authors interpreted that the facet morphology in the pathogenesis of the spondylolisthesis was a factor secondary to facet joint osteoarthritis, and was not the primary one. None dealt the effect of facet shape and laminar inclination on slippage severity. Method: The subject materials were 50 patients (10 males and 40 females) with degenerative spondylolisthesis, treated between 1999 and 2013. Simple radiograms were utilized for assessment. Facet joints were classified by Tsunoda et al., based on its developmental shape and alignment on radiograms; X, M, and W types. Also the laminar inclination and facet inclination angles were measured. Results: Among 50 patients 45 had anterolisthesis with (forward flexion instability) and only five had retrolisthesis (extension instability). In 45 cases of anterolisthesis, there were 24 "X" types, 4 "M" types, and 17 "W" types, while in 5 cases of retrolisthesis there were 3 "X" and 2 "M" types. In 45 cases of anterolisthesis, 24 with "X" type facets had Myerding's grade I slip, and one had grade II slip; Among the 4 "M" types two had grade I slip and two had grade II slip, while among 17 "W" type, there were four grade I slip, 11 grade II slip, and two grade III slip. 13 out of the 16 anterolisthesis over grade II slip had "W" type facets. Vertebra with "W" type facets had average 130° laminar inclination angle and 122° facet inclination angles, while "X" and "M" type facets had less inclination of both angles. Conclusion: The defective facet morphology and laminar inclination angle of the lower lumbar spine can be the predisposing factor of development and slip progress of the degenerative anterolisthesis.

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Gonzalez-Suarez, Ignacio, Abena B. Redwood, and Susana Gonzalo. "Loss of A-type lamins and genomic instability." Cell Cycle 8, no. 23 (December 2009): 3860–65. http://dx.doi.org/10.4161/cc.8.23.10092.

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Vigouroux, Corinne, Martine Auclair, Emmanuelle Dubosclard, Marcel Pouchelet, Jacqueline Capeau, Jean-Claude Courvalin, and Brigitte Buendia. "Nuclear envelope disorganization in fibroblasts from lipodystrophic patients with heterozygous R482Q/W mutations in the lamin A/C gene." Journal of Cell Science 114, no. 24 (December 15, 2001): 4459–68. http://dx.doi.org/10.1242/jcs.114.24.4459.

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Dunnigan-type familial partial lipodystrophy (FPLD), characterized by an abnormal body fat redistribution with insulin resistance, is caused by missense heterozygous mutations in A-type lamins (lamins A and C). A- and B-type lamins are ubiquitous intermediate filament proteins that polymerize at the inner face of the nuclear envelope. We have analyzed primary cultures of skin fibroblasts from three patients harboring R482Q or R482W mutations. These cells were euploid and able to cycle and divide. A subpopulation of these cells had abnormal blebbing nuclei with A-type lamins forming a peripheral meshwork, which was frequently disorganized. Inner nuclear membrane protein emerin, an A-type lamin-binding protein, strictly colocalized with this abnormal meshwork. Cells from lipodystrophic patients often had other nuclear envelope defects, mainly consisting of nuclear envelope herniations that were deficient in B-type lamins, nuclear pore complexes, lamina-associated protein 2 beta, and chromatin. The mechanical properties of nuclear envelopes were altered, as judged from the extensive deformations observed in nuclei from heat-shocked cells, and from the low stringency of extraction of their components. These structural nuclear alterations were caused by the lamins A/C mutations, as the same changes were introduced in human control fibroblasts by ectopic expression of R482W mutated lamin A.

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Broers, J. L., B. M. Machiels, G. J. van Eys, H. J. Kuijpers, E. M. Manders, R. van Driel, and F. C. Ramaekers. "Dynamics of the nuclear lamina as monitored by GFP-tagged A-type lamins." Journal of Cell Science 112, no. 20 (October 15, 1999): 3463–75. http://dx.doi.org/10.1242/jcs.112.20.3463.

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The behavior of chimeric proteins consisting of A-type lamins and green fluorescent protein (GFP) was studied to investigate the localization and dynamics of nuclear lamins in living cells. Cell line CHO-K1 was transfected with cDNA constructs encoding fusion proteins of lamin A-GFP, lamin Adelta10-GFP, or lamin C-GFP. In the interphase nucleus lamin-GFP fluorescence showed a perinuclear localization and incorporation into the lamina for all three constructs. Our findings show for the first time that the newly discovered lamin A 10 protein is localized to the nuclear membrane. The GFP-tagged lamins were processed and behaved similarly to the endogenous lamin molecules, at least in cells that expressed physiological levels of the GFP-lamins. In addition to the typical perinuclear localization, in the majority of transfected cells each individual A-type lamin-GFP revealed an extensive collection of branching intra- and trans-nuclear tubular structures, which showed a clear preference for a vertical orientation. Time-lapse studies of 3-D reconstructed interphase cells showed a remarkable stability in both number and location of these structures over time, while the lamina showed considerable dynamic movements, consisting of folding and indentation of large parts of the lamina. Fluorescence recovery after bleaching studies revealed a low protein turnover of both tubular and lamina-associated lamins. Repetitive bleaching of intranuclear areas revealed the presence of an insoluble intranuclear fraction of A-type lamins. Time-lapse studies of mitotic cells showed that reformation of the lamina and the tubular structures consisting of A-type lamins did not occur until after cytokinesis was completed.

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Klapper, M., K. Exner, A. Kempf, C. Gehrig, N. Stuurman, P. A. Fisher, and G. Krohne. "Assembly of A- and B-type lamins studied in vivo with the baculovirus system." Journal of Cell Science 110, no. 20 (October 15, 1997): 2519–32. http://dx.doi.org/10.1242/jcs.110.20.2519.

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We have expressed an A-type lamin (Xenopus lamin A), a probable A-type lamin (Drosophila lamin C), two B-type lamins (Xenopus lamin LI, Drosophila lamin Dmo), and two mutants of Xenopus lamin A in Sf9 cells. All proteins were synthesized at high levels resulting in formation of paracrystals with an axial repeat of 18.5-20.0 nm by A-type lamins; in contrast B-type lamins assembled into aggregates with a fibrillar ultrastructure. Of the four wild-type proteins analyzed only lamin Dmo was found in the nuclear compartment of Sf9 cells in association with the lamina whereas the three other lamins assembled into polymers localized in the cytoplasm as well as the nucleoplasm. The Xenopus lamin A mutant lacking the complete carboxy-terminal tail assembled in the cytoplasm into long filament bundles consisting of fibrils of less than 6 nm diameter. In vitro the non-helical amino-terminal head domain of lamins is required for the formation of ‘head-to-tail’ polymers. A lamin A mutant lacking this domain could be efficiently extracted from Sf9 cells with physiological buffers containing Triton X-100, demonstrating the importance of this domain for lamin assembly in vivo.

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Sullivan, Teresa, Diana Escalante-Alcalde, Harshida Bhatt, Miriam Anver, Narayan Bhat, Kunio Nagashima, Colin L. Stewart, and Brian Burke. "Loss of a-Type Lamin Expression Compromises Nuclear Envelope Integrity Leading to Muscular Dystrophy." Journal of Cell Biology 147, no. 5 (November 29, 1999): 913–20. http://dx.doi.org/10.1083/jcb.147.5.913.

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The nuclear lamina is a protein meshwork lining the nucleoplasmic face of the inner nuclear membrane and represents an important determinant of interphase nuclear architecture. Its major components are the A- and B-type lamins. Whereas B-type lamins are found in all mammalian cells, A-type lamin expression is developmentally regulated. In the mouse, A-type lamins do not appear until midway through embryonic development, suggesting that these proteins may be involved in the regulation of terminal differentiation. Here we show that mice lacking A-type lamins develop to term with no overt abnormalities. However, their postnatal growth is severely retarded and is characterized by the appearance of muscular dystrophy. This phenotype is associated with ultrastructural perturbations to the nuclear envelope. These include the mislocalization of emerin, an inner nuclear membrane protein, defects in which are implicated in Emery-Dreifuss muscular dystrophy (EDMD), one of the three major X-linked dystrophies. Mice lacking the A-type lamins exhibit tissue-specific alterations to their nuclear envelope integrity and emerin distribution. In skeletal and cardiac muscles, this is manifest as a dystrophic condition related to EDMD.

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Wojtkowiak, Janusz, and Czeslaw O. Popiel. "Inherently Linear Annular-Duct-Type Laminar Flowmeter." Journal of Fluids Engineering 128, no. 1 (September 1, 2005): 196–98. http://dx.doi.org/10.1115/1.2137347.

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Izumi, Masako, O. Anthony Vaughan, Christopher J. Hutchison, and David M. Gilbert. "Head and/or CaaX Domain Deletions of Lamin Proteins Disrupt Preformed Lamin A and C But Not Lamin B Structure in Mammalian Cells." Molecular Biology of the Cell 11, no. 12 (December 2000): 4323–37. http://dx.doi.org/10.1091/mbc.11.12.4323.

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The nuclear lamina is an important determinant of nuclear architecture. Mutations in A-type but not B-type lamins cause a range of human genetic disorders, including muscular dystrophy. Dominant mutations in nuclear lamin proteins have been shown to disrupt a preformed lamina structure in Xenopus egg extracts. Here, a series of deletion mutations in lamins A and B1 were evaluated for their ability to disrupt lamina structure in Chinese hamster ovary cells. Deletions of either the lamin A “head” domain or the C-terminal CaaX domain formed intranuclear aggregates and resulted in the disruption of endogenous lamins A/C but not lamins B1/B2. By contrast, “head-less” lamin B1 localized to the nuclear rim with no detectable effect on endogenous lamins, whereas lamin B1 CaaX domain deletions formed intranuclear aggregates, disrupting endogenous lamins A/C but not lamins B1/B2. Filter binding assays revealed that a head/CaaX domain lamin B1 mutant interacted much more strongly with lamins A/C than with lamins B1/B2. Regulated induction of this mutant in stable cell lines resulted in the rapid elimination of all detectable lamin A protein, whereas lamin C was trapped in a soluble form within the intranuclear aggregates. In contrast to results in Xenopus egg extracts, dominant negative lamin B1 (but not lamin A) mutants trapped replication proteins involved in both the initiation and elongation phases of replication but did not effect cellular growth rates or the assembly of active replication centers. We conclude that elimination of the CaaX domain in lamin B1 and elimination of either the CaaX or head domain in lamin A constitute dominant mutations that can disrupt A-type but not B-type lamins, highlighting important differences in the way that A- and B-type lamins are integrated into the lamina.

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Brooks, D. E., A. M. Komaromy, M. C. Garcia‐Fernandez, T. J. Cutler, D. A. Samuelson, and M. E. Kallberg. "Immunohistochemistry of the extracellular matrix of the normal equine lamina cribrosa." Veterinary Ophthalmology 3, no. 2-3 (June 2000): 127–32. http://dx.doi.org/10.1046/j.1463-5224.2000.3230127.x.

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Abstract Purpose To use immunohistochemical techniques to identify and localize the structural macromolecules of the extracellular matrix (ECM) of the normal adult equine lamina cribrosa in order to make comparisons to the extracellular matrix of the lamina cribrosa of horses with glaucoma. Methods Normal eyes of five adult horses between 5 and 10 years of age were fixed in 10% neutral buffered formalin and embedded in paraffin. Polyclonal rabbit‐derived antibodies against human elastin, laminin, fibrillin‐1, and collagen types I, III and IV, and polyclonal goat‐derived antibodies against collagen type VI were used as primary antibodies.Transverse and longitudinal histologic sections of the optic nerve head and lamina cribrosa were stained using several dilutions of the primary antibodies, biotinylated link antibody, horseradish peroxidase‐labeled streptavidin, and 3,3′‐diaminobenzidine as a chromogen.The immunohistochemical staining patterns were qualitatively interpreted. Results The normal adult horse lamina cribrosa labeled positively for collagen types I, III and VI, laminin, elastin and fibrillin. Collagen type VI staining of the laminar ECM was most intense, followed by labeling for collagen types III and I, respectively. Laminar blood vessels were weakly positive for laminin and slightly positive for type IV collagen. The scleral ECM of the laminar insertion zone had more intense labeling for collagen types I and VI than did the laminar plates. Conclusions The extracellular matrix of the laminar plates of the adult equine lamina cribrosa is similar to the dog as it consists of elastic and collagen fibers (with collagen types VI, III and I). Both the normal dog and horse lamina display more intense staining of collagen type VI than is found in the ECM of the normal human lamina cribrosa. The macromolecular structure of the equine lamina cribrosa suggests that it is a very resilient structure that may provide some protection to the optic nerve axons during episodes of elevated intraocular pressure.

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Kim, Hee Y., Dong S. Chung, M. Enoki, and Soon H. Hong. "Tensile and fracture properties of NiAl/Ni micro-laminated composites prepared by reaction synthesis." Journal of Materials Research 21, no. 5 (May 1, 2006): 1141–49. http://dx.doi.org/10.1557/jmr.2006.0154.

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The mechanical properties of NiAl/Ni micro-laminated composites with highly gradient microstructure have been investigated. Two types of composites with different gradient microstructures were prepared by reaction synthesis. Intermetallics of type I and type II composites mainly consisted of Al-rich Ni0.45Al0.55 with variable thickness and Ni-rich Ni0.58Al0.42 with similar thickness, respectively. As intermetallic volume fraction increased, yield strength of type II followed the rule-of-mixture well, while that of type I deviated due to the composition variation of intermetallic phases. Fracture toughness of type II was higher than that of type I, and all showed KR curves with upward curvature by large-scale bridging. Even though the relative strength of constituent phases in intermetallic/metal laminates was not constant due to the gradient microstructure, the fracture mode transition showed similar behavior to that of metal/ceramic laminates.

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Folker, Eric S., Cecilia Östlund, G. W. Gant Luxton, Howard J. Worman, and Gregg G. Gundersen. "Lamin A variants that cause striated muscle disease are defective in anchoring transmembrane actin-associated nuclear lines for nuclear movement." Proceedings of the National Academy of Sciences 108, no. 1 (December 20, 2010): 131–36. http://dx.doi.org/10.1073/pnas.1000824108.

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Mutations in LMNA, which encodes A-type lamins, result in disparate diseases, known collectively as laminopathies, that affect distinct tissues, including striated muscle and adipose tissue. Lamins provide structural support for the nucleus and sites of attachment for chromatin, and defects in these functions may contribute to disease pathogenesis. Recent studies suggest that A-type lamins may facilitate connections between the nucleus and the cytoskeleton mediated by nuclear envelope nesprin and SUN proteins. In mammalian cells, however, interfering with A-type lamins does not affect the localization of these proteins. Here, we used centrosome orientation in fibroblasts, which requires separate nuclear and centrosome positioning pathways, as a model system to understand how LMNA mutations affect nucleus-cytoskeletal connections. We find that LMNA mutations causing striated muscle diseases block actin-dependent nuclear movement, whereas most that affect adipose tissue inhibit microtubule-dependent centrosome positioning. Genetic deletion or transient depletion of A-type lamins also blocked nuclear movement, showing that mutations affecting muscle exhibit the null phenotype. Lack of A-type lamins, or expression of variants that cause striated muscle disease, did not affect assembly of nesprin-2G and SUN2 into transmembrane actin-associated nuclear (TAN) lines that attach the nucleus to retrogradely moving actin cables. Nesprin-2G TAN lines were less stable, however, and slipped over the nucleus rather than moving with it, indicating that they were not anchored. Nesprin-2G TAN lines also slipped in SUN2-depleted cells. Our results establish A-type lamins as anchors for nesprin-2G–SUN2 TAN lines to allow productive movement and proper positioning of the nucleus by actin.

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Guinde, Julien, Diane Frankel, Sophie Perrin, Valérie Delecourt, Nicolas Lévy, Fabrice Barlesi, Philippe Astoul, Patrice Roll, and Elise Kaspi. "Lamins in Lung Cancer: Biomarkers and Key Factors for Disease Progression through miR-9 Regulation?" Cells 7, no. 7 (July 16, 2018): 78. http://dx.doi.org/10.3390/cells7070078.

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Lung cancer represents the primary cause of cancer death in the world. Malignant cells identification and characterization are crucial for the diagnosis and management of patients with primary or metastatic cancers. In this context, the identification of new biomarkers is essential to improve the differential diagnosis between cancer subtypes, to select the most appropriate therapy, and to establish prognostic correlations. Nuclear abnormalities are hallmarks of carcinoma cells and are used as cytological diagnostic criteria of malignancy. Lamins (divided into A- and B-types) are localized in the nuclear matrix comprising nuclear lamina, where they act as scaffolding protein, involved in many nuclear functions, with regulatory effects on the cell cycle and differentiation, senescence and apoptosis. Previous studies have suggested that lamins are involved in tumor development and progression with opposite results concerning their prognostic role. This review provides an overview of lamins expression in lung cancer and the relevance of these findings for disease diagnosis and prognosis. Furthermore, we discuss the link between A-type lamins expression in lung carcinoma cells and nuclear deformability, epithelial to mesenchymal transition, and metastatic potential, and which mechanisms could regulate A-type lamins expression in lung cancer, such as the microRNA miR-9.

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Hennekes, H., and E. A. Nigg. "The role of isoprenylation in membrane attachment of nuclear lamins. A single point mutation prevents proteolytic cleavage of the lamin A precursor and confers membrane binding properties." Journal of Cell Science 107, no. 4 (April 1, 1994): 1019–29. http://dx.doi.org/10.1242/jcs.107.4.1019.

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Mature A- and B-type lamins differ in the extent to which they interact with the nuclear membrane and thus represent an interesting model for studying the role of isoprenylation and carboxyl-methylation in membrane attachment. Both A- and B-type lamins are isoprenylated and carboxyl-methylated shortly after synthesis, but A-type lamins undergo a further proteolytic cleavage which results in the loss of the hydrophobically modified C terminus. Here, we have constructed mutants of chicken lamin A that differ in their abilities to serve as substrates for different post-translational processing events occurring at the C terminus of the wild-type precursor. In addition to studying full-length proteins, we have analyzed C-terminal end domains of lamin A, either alone or after fusion to reporter proteins. Mutant proteins were expressed in mammalian cells, and their membrane association was analyzed by immunofluorescence microscopy and subcellular fractionation. Our results provide information on the substrate specificity and subcellular localization of the lamin-A-specific protease. Moreover, they indicate that hydrophobic modifications of the C-terminal end domains account for the differential membrane-binding properties of A- and B-type lamins. Thus, some of the integral membrane proteins implicated in anchoring B-type lamins to the membrane may function as receptors for the isoprenylated and carboxyl-methylated C terminus.

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Guénantin, Anne-Claire, Audrey Ibre, and Michel Pucéat. "Cardiomyopathie due à la lamine de type A mutée." médecine/sciences 37, no. 10 (October 2021): 836–39. http://dx.doi.org/10.1051/medsci/2021098.

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Guénantin, Anne-Claire, Audrey Ibre, and Michel Pucéat. "Cardiomyopathie due à la lamine de type A mutée." médecine/sciences 37, no. 10 (October 2021): 836–39. http://dx.doi.org/10.1051/medsci/2021098.

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32

Yang, Shao H., Hea-Jin Jung, Catherine Coffinier, Loren G. Fong, and Stephen G. Young. "Are B-type lamins essential in all mammalian cells?" Nucleus 2, no. 6 (November 2011): 562–69. http://dx.doi.org/10.4161/nucl.2.6.18085.

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Smith, Erica D., Brian A. Kudlow, Richard L. Frock, and Brian K. Kennedy. "A-type nuclear lamins, progerias and other degenerative disorders." Mechanisms of Ageing and Development 126, no. 4 (April 2005): 447–60. http://dx.doi.org/10.1016/j.mad.2004.10.006.

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34

Alsheimer, M. "Disruption of spermatogenesis in mice lacking A-type lamins." Journal of Cell Science 117, no. 7 (March 1, 2004): 1173–78. http://dx.doi.org/10.1242/jcs.00975.

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35

Zastrow, M. S. "Proteins that bind A-type lamins: integrating isolated clues." Journal of Cell Science 117, no. 7 (March 1, 2004): 979–87. http://dx.doi.org/10.1242/jcs.01102.

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36

Gonzalez-Suarez, Ignacio, and Susana Gonzalo. "Nurturing the genome: A-type lamins preserve genomic stability." Nucleus 1, no. 2 (March 1, 2010): 129–35. http://dx.doi.org/10.4161/nucl.1.2.10797.

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Muralikrishna, Bh, Jyotsna Dhawan, Nandini Rangaraj, and Veena K. Parnaik. "Distinct changes in intranuclear lamin A/C organization during myoblast differentiation." Journal of Cell Science 114, no. 22 (November 15, 2001): 4001–11. http://dx.doi.org/10.1242/jcs.114.22.4001.

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Intranuclear lamin foci or speckles have been observed in various cell types. In order to explore the possibility of changes in internal lamin organization during muscle differentiation, we have examined the appearance of A-type lamin speckles that associate with RNA splicing factor speckles in C2C12 myoblasts and myotubes. Lamin speckles were observed in dividing myoblasts but disappeared early during the course of differentiation in postmitotic myocytes, and were absent in myotubes and muscle fibers. However, no changes were seen in the typical peripheral organization of lamins A/C or B1 or in RNA splicing factor speckles. Lamin speckles were also absent in quiescent myoblasts but reappeared as cells were reactivated to enter the cell cycle. These changes were not observed in other quiescent cell types. Immunoblot analysis indicated that the abundance and migration of lamins A and C was not altered in differentiated myoblasts. When myotube or quiescent myoblast nuclei were extracted with nucleases and detergent, a uniformly stained internal lamina was revealed, indicating that lamins A/C were antigenically masked in these cells, probably owing to structural reorganization of the lamina during differentiation or quiescence. Our results suggest that muscle cell differentiation is accompanied by regulated rearrangements in the organization of the A-type lamins.

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Vester, B., A. Smith, G. Krohne, and R. Benavente. "Presence of a nuclear lamina in pachytene spermatocytes of the rat." Journal of Cell Science 104, no. 2 (February 1, 1993): 557–63. http://dx.doi.org/10.1242/jcs.104.2.557.

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The nuclear lamina is a karyoskeletal structure located at the periphery of cell nuclei. The major constituents are the lamins, which belong to the evolutionarily conserved multigene family of intermediate filament proteins. Lamins show a conspicuous cell type-specific expression pattern. The majority of somatic cells of vertebrates express A-type (lamins A and C) as well as B-type (lamins B1 and B2) lamins. Although a lamina structure has been demonstrated to be a ubiquitous component of somatic nuclei its existence in certain meiotic stages during spermatogenesis has been a matter of debate. In this study, we investigated the expression of lamins in rat spermatogenic cells using immunological and protein-chemical methods. We report on the presence of a nuclear lamina structure in rat pachytene spermatocytes. With the aid of a novel broad-reacting lamin antibody we have demonstrated the expression of a protein that is closely related, if not identical, to lamin B1.

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Ahmed, Hafiz, Ghulam Hussain, Sohail Gohar, Aaqib Ali, and Mohammed Alkahtani. "Impact Toughness of Hybrid Carbon Fiber-PLA/ABS Laminar Composite Produced through Fused Filament Fabrication." Polymers 13, no. 18 (September 10, 2021): 3057. http://dx.doi.org/10.3390/polym13183057.

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Nowadays, the components of carbon fiber-reinforced polymer composites (an important material) are directly produced with 3D printing technology, especially Fused Filament Fabrication (FFF). However, such components suffer from poor toughness. The main aim of this research is to overcome this drawback by introducing an idea of laying down a high toughness material on the 3D-printed carbon fiber-reinforced polymer composite sheet, thereby making a hybrid composite of laminar structure. To ascertain this idea, in the present study, a carbon-reinforced Polylactic Acid (C-PLA) composite sheet was initially 3D printed through FFF technology, which was then laid upon with the Acrylonitrile Butadiene Styrene (ABS), named as C-PLA/ABS hybrid laminar composite, in an attempt to increase its impact toughness. The hybrid composite was fabricated by varying different 3D printing parameters and was then subjected to impact testing. The results revealed that toughness increased by employing higher layer thickness and clad ratio, while it decreased by increasing the fill density, but remained unaffected due to any change in the raster angle. The highest impact toughness (23,465.6 kJ/m2) was achieved when fabrication was performed employing layer thickness of 0.5 mm, clad ratio of 1, fill density of 40%. As a result of laying up ABS sheet on C-PLA sheet, the toughness of resulting structure increased greatly (280 to 365%) as compared to the equivalent C-PLA structure, as expected. Two different types of distinct failures were observed during impact testing. In type A, both laminates fractured simultaneously without any delamination as a hammer hit the sample. In type B, the failure initiated with fracturing of C-PLA sheet followed by interfacial delamination at the boundary walls. The SEM analysis of fractured surfaces revealed two types of pores in the C-PLA lamina, while only one type in the ABS lamina. Further, there was no interlayer cracking in the C-PLA lamina contrary to the ABS lamina, thereby indicating greater interlayer adhesion in the C-PLA lamina.

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Pugh, G. E., P. J. Coates, E. B. Lane, Y. Raymond, and R. A. Quinlan. "Distinct nuclear assembly pathways for lamins A and C lead to their increase during quiescence in Swiss 3T3 cells." Journal of Cell Science 110, no. 19 (October 1, 1997): 2483–93. http://dx.doi.org/10.1242/jcs.110.19.2483.

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The expression of A-type lamins coincides with cell differentiation and as A-type lamins specifically interact with chromatin, a role in the regulation of differential gene expression has been suggested for A-type lamins. Using the mouse Swiss 3T3 cell line as a model, the change in two A-type lamins, lamins A and C, during cellular quiescence has been investigated. This well established model system mimics the first stages of differentiation when cells exit the cell cycle. In fact, quiescence in Swiss 3T3 cells was accompanied by a significant increase (2.6-fold) in lamin A protein levels and a smaller but reproducible increase (1.4-fold) in lamin C. These effects were fully reversible upon restimulation of the cells with serum. No effect upon lamin B levels was observed. Conversely, levels of A-type lamin mRNA decreased markedly as a result of quiescence suggesting transcriptional mechanisms are involved in the change in levels of lamins A and C. No difference in the incorporation of microinjected human lamin A into nuclei of quiescent or proliferating cells was observed. These data suggest A-type lamin binding sites were not limiting and indicated little difference between A-type lamin assembly mechanisms in quiescent and proliferating cells. The data did demonstrate lamin A and lamin C incorporation into the nuclear lamina proceeded by different pathways when microinjected in Swiss 3T3 cells. The incorporation of recombinant lamin C into the nuclear lamina was delayed compared to lamin A and proceeded via intranuclear foci. Such foci were not seen with microinjected lamin A. Instead, recombinant lamin A was rapidly (<20 minutes) incorporated into the nuclear lamina. Comicroinjection of lamin A with lamin C did not prevent foci formation but assisted in the rapid clearing (t1/2=30 minutes) of these structures and the incorporation of both lamins A and C into the lamina. These data suggest that the incorporation of lamin C into the lamina is facilitated by lamin A. They demonstrate a distinct difference in the nuclear assembly pathways of lamins A and C and show for the first time a functional distinction for these two splice variants of the A-type lamin gene. From the differences in assembly pathways and changes in protein levels accompanying quiescence in 3T3 cells, we suggest distinct roles for lamin A and lamin C in proliferating and quiescent states of the cell cycle.

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41

Andrés, Vicente, and José M. González. "Role of A-type lamins in signaling, transcription, and chromatin organization." Journal of Cell Biology 187, no. 7 (December 28, 2009): 945–57. http://dx.doi.org/10.1083/jcb.200904124.

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A-type lamins (lamins A and C), encoded by the LMNA gene, are major protein constituents of the mammalian nuclear lamina, a complex structure that acts as a scaffold for protein complexes that regulate nuclear structure and functions. Interest in these proteins has increased in recent years with the discovery that LMNA mutations cause a variety of human diseases termed laminopathies, including progeroid syndromes and disorders that primarily affect striated muscle, adipose, bone, and neuronal tissues. In this review, we discuss recent research supporting the concept that lamin A/C and associated nuclear envelope proteins regulate gene expression in health and disease through interplay with signal transduction pathways, transcription factors, and chromatin-associated proteins.

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Firmbach-Kraft, I., and R. Stick. "The role of CaaX-dependent modifications in membrane association of Xenopus nuclear lamin B3 during meiosis and the fate of B3 in transfected mitotic cells." Journal of Cell Biology 123, no. 6 (December 15, 1993): 1661–70. http://dx.doi.org/10.1083/jcb.123.6.1661.

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Recent evidence shows that the COOH-terminal CaaX motif of lamins is necessary to target newly synthesized proteins to the nuclear envelope membranes. Isoprenylation at the CaaX-cysteine has been taken to explain the different fates of A- and B-type lamins during cell division. A-type lamins, which loose their isoprenylation shortly after incorporation into the lamina structure, become freely soluble upon mitotic nuclear envelope breakdown. Somatic B-type lamins, in contrast, are permanently isoprenylated and, although depolymerized during mitosis, remain associated with remnants of nuclear envelope membranes. However, Xenopus lamin B3, the major B-type lamin of amphibian oocytes and eggs, becomes soluble after nuclear envelope breakdown in meiotic metaphase. Here we show that Xenopus lamin B3 is permanently isoprenylated and carboxyl methylated in oocytes (interphase) and eggs (meiotic metaphase). When transfected into mouse L cells Xenopus lamin B3 is integrated into the host lamina and responds to cell cycle signals in a normal fashion. Notably, the ectopically expressed Xenopus lamin does not form heterooligomers with the endogenous lamins as revealed by a coprecipitation experiment with mitotic lamins. In contrast to the situation in amphibian eggs, a significant portion of lamin B3 remains associated with membranes during mitosis. We conclude from these data that the CaaX motif-mediated modifications, although necessary, are not sufficient for a stable association of lamins with membranes and that additional factors are involved in lamin-membrane binding.

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Vadrot, Nathalie, Isabelle Duband-Goulet, Eva Cabet, Wikayatou Attanda, Alice Barateau, Patrick Vicart, Fabien Gerbal, et al. "The p.R482W substitution in A-type lamins deregulates SREBP1 activity in Dunnigan-type familial partial lipodystrophy." Human Molecular Genetics 24, no. 7 (December 18, 2014): 2096–109. http://dx.doi.org/10.1093/hmg/ddu728.

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Gou, Qiyang, and Shang Xu. "The Controls of Laminae on lacustrine Shale Oil Content in China: A Review from Generation, Retention, and Storage." Energies 16, no. 4 (February 16, 2023): 1987. http://dx.doi.org/10.3390/en16041987.

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The successful development of shale oil in China has claimed that laminated shale is a favorable lithofacies for the effective extraction of petroleum. Clarifying the role of laminae in shale oil generation, migration, storage, and enrichment is urgent and important. Starting from the describing and classifying of the lamina, the common methods and terms used to delineate lamina types are briefly summarized. The results of different schemes are often mutually inclusive, which prompted scholars to work towards a unified division scheme. The influencing factors of oil retention in shale systems, including organic matter (OM) type, total organic carbon (TOC) content, OM maturity, mineral composition, pore structure, and preservation conditions, are systematically discussed. Subsequently, comparative work on source rock quality, reservoir properties, and hydrocarbon expulsion efficiency of shales with different laminar structures is carried out. The comparison results of shale with different rock structures reveal that the laminated shale has a high expulsion efficiency. However, the strong oil generation capacity and superior storage space of laminated shale synergistically control the considerable amount of retained oil in the shale system. Especially the oil mobility of laminated shale is also considered because of great pore size and pore connectivity. The fine evaluation of laminar structure and prediction of laminar distribution has great significance for the selection of shale oil “sweet spot area” or “sweet spot interval”.

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SATO, Toshihiro, Shuji TAKASAKI, Hiroto TERASHI, Soutaro KURATA, Tomohito HONDA, Isamu MURAKAMI, Sakuhei FUJIWARA, Hiroshi SHINKAI, and Susumu TAKAYASU. "Laminin and Type VI Collagen in Dermatofibrosarcoma Protuberans." Nishi Nihon Hifuka 54, no. 3 (1992): 487–90. http://dx.doi.org/10.2336/nishinihonhifu.54.487.

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Çalış, N., Alpagut Kara, Ferhat Kara, and Hasan Mandal. "Development of Laminar Type Functionally Graded SiAlON Ceramics." Key Engineering Materials 264-268 (May 2004): 1095–98. http://dx.doi.org/10.4028/www.scientific.net/kem.264-268.1095.

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Li, H., S. H. Lubow, S. Li, and D. N. C. Lin. "TYPE I PLANET MIGRATION IN NEARLY LAMINAR DISKS." Astrophysical Journal 690, no. 1 (December 8, 2008): L52—L55. http://dx.doi.org/10.1088/0004-637x/690/1/l52.

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48

Kurovskaya, M. K. "Distribution of laminar phases at eyelet-type intermittency." Technical Physics Letters 34, no. 12 (December 2008): 1063–65. http://dx.doi.org/10.1134/s1063785008120225.

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Wang, Xiaolu, Yuchun Chen, Yuxiang Jiang, and Kai Zhang. "Research of Small Sheet-Type Laminar Flow Meter." Xibei Gongye Daxue Xuebao/Journal of Northwestern Polytechnical University 38, no. 4 (August 2020): 792–96. http://dx.doi.org/10.1051/jnwpu/20203840792.

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A small sheet-type LFM is proposed to solve the problems of leakage and deformation in the design of traditional sheet-type LFM. The pressure tap is set in the middle of the laminar flow channel to extract pressure from the fully developed laminar flow. The design value Remax·de/l is 5.81, which is much higher than the 2~2.5 required by the traditional design. Experimental results show that the linearity factor ξL of small sheet-type LFM can reach 0.81% and the accuracy is up to 1%, which shows that the present design can effectively overcome the nonlinear effects caused by sudden expansion and contraction. In addition, when the flow rate is above 20% designed maximum valve, the calculation error of pressure drop can be controlled below 5.42%.

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Rozgacheva, I. K., and E. A. Bruevich. "Model of laminar convection in solar type stars." Astronomical & Astrophysical Transactions 21, no. 1-3 (January 2002): 27–35. http://dx.doi.org/10.1080/10556790215583.

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Journal articles on the topic 'Lamines de type A'

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