Analytical and Experimental Determination of Surface Finish Effects on the EHD Performance of Ball Bearings

Russell, Thomas; Clark, John Cripps

doi:10.1080/05698197908982926

Cited by 8 publications

(13 citation statements)

References 2 publications

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“…Thus, these data argue that the membrane-bound form of Steel factor is required for proper signaling in the brain, as it is in the hematopoietic, reproductive, and melanocyte lineages (15,16). It is also possible that the remaining learning and synaptic transmission observed in Sl/Sld mice reflects the residual activity of the soluble steel factor still expressed by the Sld allele.…”

Section: Discussionmentioning

confidence: 99%

“…We examined the possible involvement of the Kit receptor tyrosine kinase in hippocampal-dependent learning. Mutations in the murine genes for either the Kit receptor [the W locus (10,11)] or its ligand Steel factor [the Steel (Sl) locus (12)(13)(14)] have deleterious effects on development of the melanocyte, germ cell, and hematopoietic lineages (15,16). As predicted from the W/Sl mutant mice phenotypes, c-kit is expressed in the three cell lineages known to be affected by W or Sl mutations, while Steel is expressed in cells located in their migratory pathways and adjacent to their final destinations (17)(18)(19)(20).…”

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confidence: 99%

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Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.

Motro

Wojtowicz

Bernstein

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

100

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Mice carrying mutations in either the dominant white-spotting (W) or Steel (Sl) loci exhibit deficits in melanogenesis, gametogenesis, and hematopoiesis. W encodes the Kit receptor tyrosine kinase, while SI encodes the Kit ligand, Steel factor, and the receptor-ligand pair are contiguously expressed at anatomical sites expected from the phenotypes of Wand Sl mice. The c-kit and Steel genes are also both highly expressed in the adult murine hippocampus: Steel is expressed in dentate gyrus neurons whose mossy fiber axons synapse with the c-kit expressing CA3 pyramidal neurons. We report here that SI/Sid mutant mice have a specific deficit in spatial learning. These mutant mice are also deficient in baseline synaptic transmission between the dentate gyrus and CA3 but show normal long-term potentiation in this pathway.These observations demonstrate a role for Steel factor/Kit signaling in the adult nervous system and suggest that a severe deficit in hippocampal-dependent learning need not be associated with reduced hippocampal long-term potentiation.Lesion analyses in rodents, monkeys, and humnans point to the critical role of hippocampal formation in a specific kind of learning and memory variously called declarative, explicit, or configural (1-3). Configural learning, defined as the processes that establish and store a representation of the relations (e.g., in space) between more than two stimuli, can be differentiated from a hippocampal-independent, simpler type of learning about the relations between two stimuli variously called procedural, implicit, or simple association learning (4). Modulation of synaptic strength has long been postulated as the central mechanism of learning and memory. In certain parts of the central nervous system, a long-term potentiation (LTP) of synaptic efficiency is observed. LTP can be induced by a brief high-frequency stimulation of afferent fibers, in both the intact animal and in tissue slices, and in most sites exhibits the specificity, cooperativity, and associativity predicted by Hebb (5-7). Although these electrophysiological characteristics of LTP make it a good candidate for the physiological mechanism of configural learning, the evidence remains equivocal (8, 9). mutants, most noticeably in certain structures of the nervous system (17, 20). For example, high levels of Steel transcripts are found in the enthorhinal cortex and dentate gyrus, while c-kit is found in the nearby CA3 and CAl pyramidal neurons and subiculum in the hippocampus (20).The contiguous high level expression of c-kit and Steel in the adult murine hippocampus suggests a possible role for the Steel factor/Kit signaling pathway in hippocampal-dependent learning and memory. To test this possibility, we used the Morris water maze task to examine the spatial learning ability of Steel mutant mice. The Morris water maze is the most commonly used test to examine deficits in configural learning tasks following damage or dysfunction in the hippocampus (21), including its mossy fiber system (22, 23). We show h...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.

Motro

Wojtowicz

Bernstein

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

100

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“…The results provide the first functional support for the intercalation theory of Cajal (2). METHODS Heterozygotes (W/+) and (WV/+) derived from C57BL/6 mice were paired to obtain +/+, W/+, WV/+, WIWv, and WV/Wv offspring (17). Animals (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) …”

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confidence: 99%

Interstitial cells of Cajal mediate inhibitory neurotransmission in the stomach.

Burns

Lomax²,

Torihashi³

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

487

741

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The structural relationships between interstitial cells of Cajal (ICC), varicose nerve fibers, and smooth muscle cells in the gastrointestinal tract have led to the suggestion that ICC may be involved in or mediate enteric neurotransmission. We characterized the distribution of ICC in the murine stomach and found two distinct classes on the basis of morphology and immunoreactivity to antibodies against c-Kit receptors. ICC with multiple processes formed a network in the myenteric plexus region from corpus to pylorus. Spindle-shaped ICC were found within the circular and longitudinal muscle layers (IC-IM) throughout the stomach. The density of these cells was greatest in the proximal stomach. IC-IM ran along nerve fibers and were closely associated with nerve terminals and adjacent smooth muscle cells. IC-IM failed to develop in mice with mutations in c-kit. Therefore, we used W/WV mutants to test whether IC-IM mediate neural inputs in muscles of the gastric fundus. The distribution of inhibitory nerves in the stomachs of c-kit mutants was normal, but NO-dependent inhibitory neuroregulation was greatly reduced. Smooth muscle tissues of W/Wv mutants relaxed in response to exogenous sodium nitroprusside, but the membrane potential effects of sodium nitroprusside were attenuated. These data suggest that IC-IM play a critical serial role in NO-dependent neurotransmission: the cellular mechanism(s) responsible for transducing NO into electrical responses may be expressed in IC-IM. Loss of these cells causes loss of electrical responsiveness and greatly reduces responses to nitrergic nerve stimulation.Ramon y Cajal observed cells at the terminus of the autonomic nervous system in the acini of salivary glands, in the connective tissue of the pancreas, between the glands of Lieberkuhn, in the intestinal villi, and within the tunica muscularis of the gastrointestinal (GI) tract (1). The processes of cells in the GI tract, which became known as interstitial cells of Cajal (ICC), form a network that is intercalated between nerve terminals and effector cells. Cajal believed that the structures he identified were essential elements in peripheral neurotransmission (2), and this hypothesis has been investigated for the past century (3). ICC were later recognized to be nonneural (4), but their anatomical locations in the GI tract continue to suggest a role for these cells in neurotransmission (3,5 Recently, it was shown that mutations in c-kit, a protooncogene located at the W locus on chromosome 5 in the mouse that encodes a receptor tyrosine kinase (10), or in stem cell factor, the natural ligand for c-Kit receptors, result in developmental defects in some classes of . For example, ICC in the myenteric plexus region (IC-MY) of the small intestine are greatly decreased in numbers in these mutants and slow waves are abolished, confirming a role for IC-MY as pacemakers (3,15,16). ICC in the region of the deep muscular plexus, however, were unaffected by defects in the c-Kit signaling pathway (14). Loss of IC-MY did not af...

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“…Kit is encoded by the murine White Spotting (W) locus (5,6) and controls various cellular events during development and in adult life. Mutations at the W locus result in defects in gametogenesis, melanogenesis, and hematopoiesis (7,8). The hematopoietic defects include macrocytic anemia (8) and the virtual absence of tissue mast cells (9).…”

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confidence: 99%

“…Mutations at the W locus result in defects in gametogenesis, melanogenesis, and hematopoiesis (7,8). The hematopoietic defects include macrocytic anemia (8) and the virtual absence of tissue mast cells (9). Kit is expressed on both mature MCs and their earliest progenitors (10) as well as on cells of erythroid and melanocytic lineages and on germ cells (11).…”

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confidence: 99%

Impaired Kit- but Not FcεRI-initiated Mast Cell Activation in the Absence of Phosphoinositide 3-Kinase p85α Gene Products

Lu-Kuo¹,

Fruman²,

Joyal³

et al. 2000

Journal of Biological Chemistry

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The class I A phosphoinositide 3-kinases (PI3Ks) consist of a 110-kDa catalytic domain and a regulatory subunit encoded by the p85␣, p85␤, or p55␥ genes. We have determined the effects of disrupting the p85␣ gene on the responses of mast cells stimulated by the cross-linking of Kit and Fc⑀RI, receptors that reflect innate and adaptive responses, respectively. The absence of p85␣ gene products partially inhibited Kit ligand/stem cell factor-induced secretory granule exocytosis, proliferation, and phosphorylation of the serine/threonine kinase Akt. In contrast, p85␣ gene products were not required for Fc⑀RI-initiated exocytosis and phosphorylation of Akt. LY294002, which inhibits all classes of PI3Ks, strongly suppressed Kit-and Fc⑀RI-induced responses in p85␣ ؊/؊ mast cells, revealing the contribution of another PI3K family member(s). In contrast to B lymphocytes, mast cell proliferation was not dependent on Bruton's tyrosine kinase, a downstream effector of PI3K, revealing a distinct pathway of PI3K-dependent proliferation in mast cells. Our findings represent the first example of receptor-specific usage of different PI3K family members in a single cell type. In addition, because Kit-but not Fc⑀RI-initiated signaling is associated with mast cell proliferation, the results provide evidence that distinct biologic functions signaled by these two receptors may reflect differential usage of PI3Ks.Mast cells (MCs) 1 are functionally dynamic effector cells of innate and adaptive immunity (1). Two MC surface receptors, namely, the Kit receptor (the product of the c-kit proto-oncogene) and the high affinity receptor for IgE (Fc⑀RI), provide activation via innate and adaptive immune mechanisms, respectively (2-4). Kit is a receptor tyrosine kinase belonging to the colony-stimulating factor-1/platelet-derived growth factor receptor subfamily (3). Kit is encoded by the murine White Spotting (W) locus (5, 6) and controls various cellular events during development and in adult life. Mutations at the W locus result in defects in gametogenesis, melanogenesis, and hematopoiesis (7,8). The hematopoietic defects include macrocytic anemia (8) and the virtual absence of tissue mast cells (9). Kit is expressed on both mature MCs and their earliest progenitors (10) as well as on cells of erythroid and melanocytic lineages and on germ cells (11). Kit ligand (KL; also known as stem cell factor), is expressed in membrane-associated and soluble forms (12) by mast cells (13), fibroblasts (11), endothelial cells (14), stromal cells (15), keratinocytes (16), neuroblastoma cells (17), and tumor cell lines (18). Although KL represents a major growth and differentiation factor for both murine and human MCs (19,20), it also promotes Kit-dependent MC mediator release (21-23), as well as enhances the release of MC mediators via IgE-dependent mechanisms (22,24). Fc⑀RI belongs to the antigen receptor superfamily (4). Rodent Fc⑀RI is a tetrameric receptor consisting of an ␣ chain, ␤ chain, and a dimer of disulfide-linked ␥ chains, whereas human Fc⑀...

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Analytical and Experimental Determination of Surface Finish Effects on the EHD Performance of Ball Bearings

Cited by 8 publications

References 2 publications

Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.

Steel mutant mice are deficient in hippocampal learning but not long-term potentiation.

Interstitial cells of Cajal mediate inhibitory neurotransmission in the stomach.

Impaired Kit- but Not FcεRI-initiated Mast Cell Activation in the Absence of Phosphoinositide 3-Kinase p85α Gene Products

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