Journal articles: 'VIP'

1

Oehr, Christian. "Sehr geehrte VIP-Leserinnen und VIP-Leserinnen und VIP-Leser." Vakuum in Forschung und Praxis 17, no. 5 (October 2005): 243. http://dx.doi.org/10.1002/vipr.200590058.

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Силаева, Анна, Anna Silaeva, Нелли Чхиквадзе, Nelli Chkhikvadze, Елена Коновалова, and Elena Konovalova. "Vip-tourism marketing organization in russia." Services in Russia and abroad 8, no. 6 (December 2, 2014): 86–96. http://dx.doi.org/10.12737/6716.

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In the article is regarded the VIP-tourism marketing as an economic process, the main marketing functions in tourism sphere are underlined. More it tells us about the tourism sphere characteristic as an object for researching. It contents the general tourism service features of VIP level, it’s necessary to take it’s in account on doing marketing researches. Also the article is contents the successful VIP-tourism rules. The individual treatment to any client on such type of the tourist product formation and realization has been mentioned with special attention. The VIP-tourism question theory is confirmed in this article with leading Russian companies experience examples. Also the authors are summarized the research problems in order to organize the VIP-tourism marketing.

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&NA;. "VIP." Inpharma Weekly &NA;, no. 826 (February 1992): 7. http://dx.doi.org/10.2165/00128413-199208260-00011.

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Nachiappan, Nachiappan Chidambaram, Haibo Zhang, Jihyun Ryoo, Niranjan Soundararajan, Anand Sivasubramaniam, Mahmut T. Kandemir, Ravi Iyer, and Chita R. Das. "VIP." ACM SIGARCH Computer Architecture News 43, no. 3S (January 4, 2016): 655–67. http://dx.doi.org/10.1145/2872887.2750382.

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5

Oswald, Dieter. "Liebe VIP - Leserinnen, liebe VIP-Leser." Vakuum in Forschung und Praxis 16, no. 5 (October 2004): 219. http://dx.doi.org/10.1002/vipr.200490030.

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6

Fung, Candice, Petra Unterweger, Laura J. Parry, Joel C. Bornstein, and Jaime P. P. Foong. "VPAC1 receptors regulate intestinal secretion and muscle contractility by activating cholinergic neurons in guinea pig jejunum." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 9 (May 1, 2014): G748—G758. http://dx.doi.org/10.1152/ajpgi.00416.2013.

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In the gastrointestinal tract, vasoactive intestinal peptide (VIP) is found exclusively within neurons. VIP regulates intestinal motility via neurally mediated and direct actions on smooth muscle and secretion by a direct mucosal action, and via actions on submucosal neurons. VIP acts via VPAC1 and VPAC2 receptors; however, the subtype involved in its neural actions is unclear. The neural roles of VIP and VPAC1 receptors (VPAC1R) were investigated in intestinal motility and secretion in guinea pig jejunum. Expression of VIP receptors across the jejunal layers was examined using RT-PCR. Submucosal and myenteric neurons expressing VIP receptor subtype VPAC1 and/or various neurochemical markers were identified immunohistochemically. Isotonic muscle contraction was measured in longitudinal muscle-myenteric plexus preparations. Electrogenic secretion across mucosa-submucosa preparations was measured in Ussing chambers by monitoring short-circuit current. Calretinin+ excitatory longitudinal muscle motor neurons expressed VPAC1R. Most cholinergic submucosal neurons, notably NPY+ secretomotor neurons, expressed VPAC1R. VIP (100 nM) induced longitudinal muscle contraction that was inhibited by TTX (1 μM), PG97–269 (VPAC1 antagonist; 1 μM), and hyoscine (10 μM), but not by hexamethonium (200 μM). VIP (50 nM)-evoked secretion was depressed by hyoscine or PG97–269 and involved a small TTX-sensitive component. PG97–269 and TTX combined did not further depress the VIP response observed in the presence of PG97–269 alone. We conclude that VIP stimulates ACh-mediated longitudinal muscle contraction via VPAC1R on cholinergic motor neurons. VIP induces Cl− secretion directly via epithelial VPAC1R and indirectly via VPAC1R on cholinergic secretomotor neurons. No evidence was obtained for involvement of other neural VIP receptors.

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7

NAGAI, Katsuya. "Role of VIP-neurons in the hypothalamic suprachiasmatic nucleus in the control of blood glucose." Folia Pharmacologica Japonica 123, no. 4 (2004): 253–60. http://dx.doi.org/10.1254/fpj.123.253.

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8

Pulker, H. K. "Sehr geehrte VIP-Leserinnen und VIP-Leser." Vakuum in Forschung und Praxis 17, no. 4 (August 2005): 183. http://dx.doi.org/10.1002/vipr.200590045.

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9

Lee, Sang-Hun, and Charles L. Cox. "Excitatory Actions of Vasoactive Intestinal Peptide on Mouse Thalamocortical Neurons Are Mediated by VPAC2 Receptors." Journal of Neurophysiology 96, no. 2 (August 2006): 858–71. http://dx.doi.org/10.1152/jn.01115.2005.

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Thalamic nuclei can generate intrathalamic rhythms similar to those observed at various arousal levels and pathophysiological conditions such as absence epilepsy. These rhythmic activities can be altered by a variety of neuromodulators that arise from brain stem regions as well as those that are intrinsic to the thalamic circuitry. Vasoactive intestinal peptide (VIP) is a neuropeptide localized within the thalamus and strongly attenuates intrathalamic rhythms via an unidentified receptor subtype. We have used transgenic mice lacking a specific VIP receptor, VPAC2, to identify its role in VIP-mediated actions in the thalamus. VIP strongly attenuated both the slow, 2–4 Hz and spindle-like 5–8 Hz rhythmic activities in slices from wild-type mice (VPAC2+/+) but not in slices from VPAC2 receptor knock-out mice (VPAC2−/−), which suggests a major role of VPAC2 receptors in the antioscillatory actions of VIP. Intracellular recordings revealed that VIP depolarized all relay neurons tested from VPAC2+/+ mice. In VPAC2−/− mice, however, VIP produced no membrane depolarization in 80% of neurons tested. In relay neurons from VPAC2+/+ mice, VIP enhanced the hyperpolarization-activated mixed cation current, Ih, via cyclic AMP activity, but VIP did not alter Ih in VPAC2−/− mice. In VPAC2−/− mice, pituitary adenylate cyclase activating-polypeptide (PACAP) depolarized the majority of relay neurons via Ih enhancement presumably via PAC1 receptor activation. Our findings suggest that VIP-mediated actions are predominantly mediated by VPAC2 receptors, but PAC1 receptors may play a minor role. The excitatory actions of VIP and PACAP suggest these peptides may not only regulate intrathalamic rhythmic activities, but also may influence information transfer through thalamocortical circuits.

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10

Kakaraparthy, Aarati, Jignesh M. Patel, Brian P. Kroth, and Kwanghyun Park. "VIP hashing." Proceedings of the VLDB Endowment 15, no. 10 (June 2022): 1978–90. http://dx.doi.org/10.14778/3547305.3547306.

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All data is not equally popular. Often, some portion of data is more frequently accessed than the rest, which causes a skew in popularity of the data items. Adapting to this skew can improve performance, and this topic has been studied extensively in the past for disk-based settings. In this work, we consider an in-memory data structure, namely hash table , and show how one can leverage the skew in popularity for higher performance. Hashing is a low-latency operation, sensitive to the effects of caching and code complexity, among other factors. These factors make learning in-the-loop challenging as the overhead of performing additional operations can have significant impact on performance. In this paper, we propose VIP hashing, a hash table method that uses lightweight mechanisms for learning the skew in popularity and adapting the hash table layout on the fly. These mechanisms are non-blocking, i.e, the hash table is operational at all times. The overhead is controlled by sensing changes in the popularity distribution to dynamically switch-on/off the mechanisms as needed. We ran extensive tests against a host of workloads generated by Wiscer , a homegrown benchmarking tool, and we find that VIP hashing improves performance in the presence of skew (22% increase in fetch operation throughput for a hash table with 1M keys under low skew) while adapting to insert and delete operations, and changing popularity distribution of keys on the fly. Our experiments on DuckDB show that VIP hashing reduces the end-to-end execution time of TPC-H query 9 by 20% under low skew.

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11

Krause, Frank-Lothar, and Ralph Schultz. "ViP-RoaM." ZWF Zeitschrift für wirtschaftlichen Fabrikbetrieb 98, no. 6 (June 28, 2003): 266–67. http://dx.doi.org/10.3139/104.030607.

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12

Haworth, Alan. "The VIP." Philosophers' Magazine, no. 22 (2003): 43–45. http://dx.doi.org/10.5840/tpm20032286.

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Shao, Zhou, Muhammad Aamir Cheema, David Taniar, and Hua Lu. "VIP-Tree." Proceedings of the VLDB Endowment 10, no. 4 (November 2016): 325–36. http://dx.doi.org/10.14778/3025111.3025115.

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14

Guglielmo, B. Joseph. "Vip News." Annals of Pharmacotherapy 40, no. 3 (March 2006): 587. http://dx.doi.org/10.1345/aph.1n104.

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Nahata, Milap. "Vip News." Annals of Pharmacotherapy 43, no. 9 (July 21, 2009): 1549. http://dx.doi.org/10.1345/aph.1n139.

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Kehoe, William A. "Vip News." Annals of Pharmacotherapy 43, no. 9 (August 18, 2009): 1549. http://dx.doi.org/10.1345/aph.1n140.

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17

Gilks, Megan. "Vip Holidays." British Journal of Visual Impairment 14, no. 1 (January 1996): 42–43. http://dx.doi.org/10.1177/026461969601400115.

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18

Schroeder, Donna, Joseph F. Dasta, and Barbara Z. Zarowitz. "Vip News." Annals of Pharmacotherapy 29, no. 7-8 (July 1995): 814. http://dx.doi.org/10.1177/106002809502907-840.

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19

Hamilton, Angela S. "VIP treatment." Practice Development in Health Care 5, no. 4 (2006): 183–84. http://dx.doi.org/10.1002/pdh.202.

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20

Fishbein, V. A., D. H. Coy, S. J. Hocart, N.-Y. Jiang, J. E. Mrozinski, S. A. Mantey, and R. T. Jensen. "A chimeric VIP-PACAP analogue but not VIP pseudopeptides function as VIP receptor antagonists." Peptides 15, no. 1 (January 1994): 95–100. http://dx.doi.org/10.1016/0196-9781(94)90176-7.

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21

Schulzke, J. D., E. O. Riecken, and M. Fromm. "Distension-induced electrogenic Cl- secretion is mediated via VIP-ergic neurons in rat rectal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 5 (May 1, 1995): G725—G731. http://dx.doi.org/10.1152/ajpgi.1995.268.5.g725.

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Distension of rat rectal colon causes electrogenic Cl- secretion via the plexus submucosus Meissner. This study aimed to identify the neurotransmitter(s) of this reflex pathway. Distension was applied to partially stripped rat rectal colon in Ussing chambers. Baseline short-circuit current (Isc) increased and then slowly declined again within 30 min. The increase in Isc 10 min after distension (delta Isc10) was 1.8 +/- 0.3 mumol.h-1.cm-2. Atropine (1 microM) did not alter delta Isc10. Thus cholinergic neurons with muscarinic synapses were not involved. Tissues were then desensitized to vasoactive intestinal peptide (VIP) or substance P. This required continuous infusion of VIP or substance P into the chamber; otherwise, desensitization was only temporary due to rapid degradation of VIP or substance P. During substance P desensitization, distension still induced a secretory response (delta Isc10 not significant vs. control), whereas during VIP desensitization distension no longer had an effect. Furthermore, a polyclonal anti-VIP antiserum blocked 81% and the VIP antagonist [p-Cl-D-Phe6,Leu17]VIP blocked 89% of the distension-induced delta Isc10, supporting the results of the desensitization experiments. To localize the site of VIP action, tetrodotoxin (TTX) was used. The TTX effect on Isc during VIP stimulation was not different from its effect on baseline Isc. This is in accord with the concept that the VIP receptors are mainly located on the enterocytes. We conclude that VIP, but not substance P or acetylcholine (via muscarinic receptors), acts as a neurotransmitter in the distension-induced reflex pathway, causing Cl- secretion in rat rectal colon.

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22

Wilkins, Brad W., Linda H. Chung, Nathan J. Tublitz, Brett J. Wong, and Christopher T. Minson. "Mechanisms of vasoactive intestinal peptide-mediated vasodilation in human skin." Journal of Applied Physiology 97, no. 4 (October 2004): 1291–98. http://dx.doi.org/10.1152/japplphysiol.00366.2004.

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Vasoactive intestinal peptide (VIP) is known to induce histamine release in human skin and to include a nitric oxide (NO)-dependent dilation in several other vascular beds. However, the relative contribution of histamine and NO to VIP-mediated vasodilation in human skin is unknown. Forty-three subjects volunteered to participate in two studies designed to examine the mechanism of VIP-mediated vasodilation in human skin. Study 1 examined the contribution of NO in the skin blood flow response to eight doses of VIP ranging from 25 to 800 pmol. In addition, study 1 examined a specific role for NO in VIP-mediated dilation. Study 2 examined the relative contribution of NO and histamine to VIP-mediated dilation via H1 and H2 histamine receptors. Infusions were administered to skin sites via intradermal microdialysis. Red blood cell flux was measured by using laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was calculated and normalized to maximal vasodilation. VIP-mediated vasodilation includes a NO-dependent component at doses above 100 pmol, where NO synthase inhibition significantly attenuates CVC ( P < 0.05). Inhibition of H1 receptors attenuates the rise in CVC to exogenous VIP ( P < 0.05); however, combined H1-receptor inhibition and NO synthase inhibition further reduced VIP-mediated vasodilation compared with either H1 inhibition or NO synthase inhibition alone ( P < 0.05). In contrast to H1-receptor inhibition, H2-receptor inhibition did not affect vasodilation to exogenous VIP. Thus, in human skin, VIP-mediated vasodilation includes a NO-dependent component that could not be explained by H1- and H2-receptor activation.

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Brown, T. M., C. S. Colwell, J. A. Waschek, and H. D. Piggins. "Disrupted Neuronal Activity Rhythms in the Suprachiasmatic Nuclei of Vasoactive Intestinal Polypeptide-Deficient Mice." Journal of Neurophysiology 97, no. 3 (March 2007): 2553–58. http://dx.doi.org/10.1152/jn.01206.2006.

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Vasoactive intestinal polypeptide (VIP), acting via the VPAC2 receptor, is a key signaling pathway in the suprachiasmatic nuclei (SCN), the master clock controlling daily rhythms in mammals. Most mice lacking functional VPAC2 receptors are unable to sustain behavioral rhythms and lack detectable SCN electrical rhythms in vitro. Adult mice that do not produce VIP (VIP/PHI−/−) exhibit less severe alterations in wheel-running rhythms, but the effects of this deficiency on the amplitude, phasing, or periodicity of their SCN cellular rhythms are unknown. To investigate this, we used suction electrodes to extracellularly record multiple- and single-unit electrical activity in SCN brain slices from mice with varying degrees of VIP deficiency, ranging from wild-type (VIP/PHI+/+) to heterozygous (VIP/PHI+/−) and VIP/PHI−/− animals. We found decreasing proportions of rhythmic cells in SCN slices from VIP/PHI+/+ (∼91%, n = 23) through VIP/PHI-/+ (∼71%, n = 28) to VIP/PHI−/− mice (62%; n = 37) and a parallel trend toward decreasing amplitude in the remaining rhythmic cells. SCN neurons from VIP/PHI−/− mice exhibited a broad range in the period and phasing of electrical rhythms, concordant with the known alterations in their behavioral rhythms. Further, treatment of VIP/PHI−/− slices with a VPAC2 receptor antagonist significantly reduced the proportion of oscillating neurons, suggesting that VPAC2 receptors still become activated in the SCN of these mice. The results establish that VIP is important for appropriate periodicity and phasing of SCN neuronal rhythms and suggest that residual VPAC2 receptor signaling promotes rhythmicity in adult VIP/PHI−/− mice.

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Leite, Aline Chaves, Eduarda Tavares Garcia, Ingrid Rezende Silva Palacios, Jhonathan Carvalho da Silveira, Valéria Cristine Pereira Gomes, and Myriam Angélica Dornelas. "Plano de negócios: VIP fungi / Business plan: VIP fungi." Brazilian Journal of Development 8, no. 5 (May 5, 2022): 34651–73. http://dx.doi.org/10.34117/bjdv8n5-132.

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Kim, Donghoon, and Luri Lee. "When VIP Status Falters: Customer Purchase Response to Changes in VIP Status and Preferential Treatment." JOURNAL OF KOREAN MARKETING ASSOCIATION 32, no. 3 (August 31, 2017): 45–68. http://dx.doi.org/10.15830/kmr.2017.32.3.45.

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Fernández, M., F. Sánchez-Franco, N. Palacios, I. Sánchez, and L. Cacicedo. "IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1." Journal of Molecular Endocrinology 34, no. 3 (June 2005): 699–712. http://dx.doi.org/10.1677/jme.1.01703.

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In previous studies we demonstrated that vasoactive intestinal peptide (VIP) mediation, and interactions between mitogen-activated protein kinase (MAPK) and cAMP/protein kinase A (PKA) signaling pathways are implicated in insulin-like growth factor I (IGF-I)- and VIP-induced lactotroph proliferation. These facts led us to investigate the intracellular mechanisms involved in IGF-I- and VIP-induced lactotroph proliferation. Exposure of cultured male rat pituitary cells to IGF-I (10−7 M) or VIP (10−7 M) stimulated the MAPK cascade. Studies in GH4C1 cells, with an expression vector for Rap1 GTPase-activating protein (Rap1 GAP1), demonstrated reduced VIP-induced MAPK activation, indicating that VIP-dependent activation of the extracellular signal-regulated kinase (ERK) pathway requires PKA-Rap1 signaling. IGF-I induced cAMP-response element (CRE)-binding protein (CREB) phosphorylation through the Ras-MAPK pathway, whereas VIP phosphorylated CREB directly via PKA. The mechanisms that regulate IGF-I-and VIP-CREB-dependent gene transcription were examined using GH4C1 cells transiently transfected with a CRE reporter gene. IGF-I and VIP stimulation of CRE-mediated transcription required activation of both Ras-MAPK and cAMP/PKA signaling. This activation was blocked in the presence of Rap1 GAP1. In summary, we showed that IGF-I and VIP stimulated MAPK activity and the phosphorylation of CREB in pituitary cells. Furthermore, VIP-dependent activation of PKA-Rap1-ERK pathways mediated VIP and IGF-I effects on CREB-dependent transcription in GH4C1 cells. Thus, it is possible that VIP- and IGF-I-induced lactotroph proliferation may involve Rap1.

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Sekizawa, K., J. Tamaoki, P. D. Graf, and J. A. Nadel. "Modulation of cholinergic neurotransmission by vasoactive intestinal peptide in ferret trachea." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2433–37. http://dx.doi.org/10.1152/jappl.1988.64.6.2433.

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We studied the effect of vasoactive intestinal peptide (VIP) on the contractile responses to electrical field stimulation (EFS) in isolated ferret tracheal segments. VIP did not change resting tension up to 2 X 10(-7) M, but it showed a biphasic effect on the responses to EFS. In concentrations up to 10(-9) M, VIP potentiated the response; at higher concentrations VIP reduced responses. Thus, at a concentration of 10(-9) M, VIP decreased the mean (+/- SE) log EFS frequency, producing 50% of maximum contraction significantly from a control value of 0.476 +/- 0.062 to 0.214 +/- 0.057 Hz (P less than 0.01); at a concentration of 2 X 10(-7) M VIP increased the half-maximal frequency from a control value of 0.513 +/- 0.086 to 0.752 +/- 0.053 Hz (P less than 0.05). The potentiating effect of VIP (10(-9) M) was not inhibited by hexamethonium, indomethacin, pyrilamine, methysergide, or [D-Pro2,D-Trp7,9] substance P. The inhibitory effect of VIP (2 X 10(-7) M) was also not inhibited by hexamethonium, indomethacin, or naloxone. In contrast to EFS-induced contraction, contractions produced by acetylcholine (10(-9) to 10(-3) M) were not affected by VIP at concentrations of 10(-9) and 2 X 10(-7) M. These results suggest that VIP modulates contractions produced by EFS via presynaptic cholinergic mechanisms and probably through a specific VIP receptor.

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Leuchte, Hanno H., Christoph Prechtl, Jens Callegari, Tobias Meis, Shani Haziraj, Dorian Bevec, and Jürgen Behr. "Augmentation of the effects of vasoactive intestinal peptide aerosol on pulmonary hypertension via coapplication of a neutral endopeptidase 24.11 inhibitor." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 6 (March 15, 2015): L563—L568. http://dx.doi.org/10.1152/ajplung.00317.2014.

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A deficiency of the pulmonary vasodilative vasoactive intestinal peptide (VIP) has been suggested to be involved in the pathophysiology of pulmonary hypertension (PH). Supplementation of VIP as an aerosol is hampered by the fact that it is rapidly inactivated by neutral endopeptidases (NEP) located on the lung surface. Coapplication of thiorphan, an NEP 24.11 inhibitor, could augment the biological effects of inhaled VIP alone. A stable pulmonary vasoconstriction with a threefold increase of pulmonary artery pressure was established by application the thromboxane mimetic U46619 in the isolated rabbit lung model. VIP and thiorphan were either applied intravascularly or as an aerosol. VIP caused a significant pulmonary vasodilation either during intravascular application or inhalation. These effects were of short duration. Thiorphan application had no effects on pulmonary vasoconstriction per se but significantly augmented the effects of VIP aerosol. Thiorphan, not only augmented the maximum hemodynamic effects of VIP aerosol, but also led to a significant prolongation of these effects. VIP causes pulmonary vasodilation in a model of acute experimental PH. The hemodynamic effects of VIP aerosol can be significantly augmented via coapplication of an NEP inhibitor.

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Nicol, MR, VJ Cobb, BC Williams, SD Morley, SW Walker, and JI Mason. "Vasoactive intestinal peptide (VIP) stimulates cortisol secretion from the H295 human adrenocortical tumour cell line via VPAC1 receptors." Journal of Molecular Endocrinology 32, no. 3 (June 1, 2004): 869–77. http://dx.doi.org/10.1677/jme.0.0320869.

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Vasoactive intestinal peptide (VIP) shows a wide tissue distribution and exerts numerous physiological actions. VIP was shown in a dose-dependent manner to increase cortisol secretion in the NCI-H295R human adrenocortical carcinoma (H295) cell line (threshold dose 3.3x10(-10) M, maximal dose 10(-7) M), coupled with a parallel increase in cAMP accumulation. Receptor-specific agonists were employed to determine which of the two known VIP receptor subtypes was involved in cortisol secretion. Treatment with the VPAC1 receptor agonist, [K(15), R(16), L(27)]VIP(1-7)/GRF(8-27), produced a dose-dependent increase in H295 cell cortisol secretion (threshold dose 10(-11) M, maximal dose 10(-7) M) similar to that seen with VIP. Meanwhile, the high-affinity VPAC2 receptor agonist, RO-25-1553, failed to stimulate significantly cortisol or cAMP production from H295 cells. Inhibition of VIP-mediated H295 cell cortisol secretion by PG97-269, a competitive VPAC1-specific antagonist, produced parallel shifts of the dose-response curve and a Schild regression slope of 0.99, indicating competitive inhibition at a single receptor subtype. VIP is known also to interact with the PAC1 receptor, albeit with lower affinity (EC(50) of approximately 200 nM) than the homologous ligand, PACAP (EC(50) of approximately 0.5 nM). PACAP stimulated cortisol secretion from H295 cells (EC(50) of 0.3 nM), suggesting the presence of functional PAC1 receptors. However, stimulation of cortisol secretion by nanomolar concentrations of VIP (EC(50) of 5 nM), coupled with real-time PCR estimation that VPAC1 receptor transcripts appear 1000-fold more abundant than PAC1 transcripts in H295 cells, makes it unlikely that VIP signals via PAC1 receptors. Together, these data suggest that VIP directly stimulates cortisol secretion from H295 cells via activation of the VPAC1 receptor subtype.

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Lau, John H., S. W. Ricky Lee, Stephen H. Pan, and Chris Chang. "Nonlinear-Time-Dependent Analysis of Micro Via-In-Pad Substrates for Solder Bumped Flip Chip Applications." Journal of Electronic Packaging 124, no. 3 (July 26, 2002): 205–11. http://dx.doi.org/10.1115/1.1462626.

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An elasto-plastic-creep analysis of a low-cost micro via-in-pad (VIP) substrate for supporting a solder bumped flip chip in a chip scale package (CSP) format which is soldered onto a printed circuit board (PCB) is presented in this study. Emphasis is placed on the design, materials, and reliability of the micro VIP substrate and of the micro VIP CSP solder joints on PCB. The solder is assumed to obey Norton’s creep law. Cross-sections of samples are examined for a better understanding of the solder bump, CSP substrate redistribution, micro VIP, and solder joint. Also, the thermal cycling test results of the micro VIP CSP PCB assembly is presented.

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Kreuzpointner, Michaela. "VIP-Betreuung inklusive." working@office 9, no. 1 (January 2008): 8–10. http://dx.doi.org/10.1007/bf03249680.

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Vetter, Bernhard. "Die VIP-Tür." agrarzeitung 76, no. 35 (2021): 2. http://dx.doi.org/10.51202/1869-9707-2021-35-002-2.

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Vetter, Bernhard. "Die VIP-Tür." agrarzeitung 76, no. 35 (2021): 2. http://dx.doi.org/10.51202/1869-9707-2021-35-002-2.

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Bartalucci, S., S. Bertolucci, M. Bragadireanu, M. Catti, M. Carnielli, C. Curceanu (Petrascu), S. Di Matteo, et al. "The VIP experiment." Journal of Physics: Conference Series 174 (June 1, 2009): 012065. http://dx.doi.org/10.1088/1742-6596/174/1/012065.

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Shaughnessy, Paul, and Jonathan Tinker. "The VIP Program." Oncology Issues 29, no. 4 (July 2014): 38–45. http://dx.doi.org/10.1080/10463356.2014.11883951.

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Gough, N. R. "Tubing with VIP." Science Signaling 7, no. 341 (September 2, 2014): ec236-ec236. http://dx.doi.org/10.1126/scisignal.2005856.

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Cong, Yali, Linying Hu, and James Dwyer. "The VIP Floors." Hastings Center Report 35, no. 1 (2005): 16–17. http://dx.doi.org/10.1353/hcr.2005.0002.

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Gozes, I., M. Fridkin, and D. E. Brenneman. "Stearyl-Nle17-VIP." Drugs of the Future 20, no. 7 (1995): 680. http://dx.doi.org/10.1358/dof.1995.020.07.305786.

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Scherle, J. "20 Jahre ViP." Vakuum in Forschung und Praxis 20, no. 2 (April 2008): 6–7. http://dx.doi.org/10.1002/vipr.200800350.

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Rafelson, William M., and Vijay Rajput. "VIP and UIP." JAMA 308, no. 6 (August 8, 2012): 579. http://dx.doi.org/10.1001/jama.2012.8727.

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Eder, Manfred. "VIP - Tender Model for Infrastructure Projects / VIP - Vergabemodell für Infrastrukturprojekte." Geomechanics and Tunnelling 5, no. 6 (December 2012): 708–17. http://dx.doi.org/10.1002/geot.201200058.

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Wang, Baowen, Zhihui Li, Xinglai Qi, Nairong Chen, Qinzhi Zeng, Dasong Dai, Mizi Fan, and Jiuping Rao. "Thermal insulation properties of green vacuum insulation panel using wood fiber as core material." BioResources 14, no. 2 (March 6, 2019): 3339–51. http://dx.doi.org/10.15376/biores.14.2.3339-3351.

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Wood fibers were prepared as core materials for a vacuum insulation panel (VIP) via a dry molding process. The morphology of the wood fibers and the microstructure, pore structure, transmittance, and thermal conductivity of the wood fiber VIP were tested. The results showed that the wood fibers had excellent thermal insulation properties and formed a porous structure by interweaving with one another. The optimum bulk density that led to a low-cost and highly thermally efficient wood fiber VIP was 180 kg/m3 to 200 kg/m3. The bulk density of the wood fiber VIP was 200 kg/m3, with a high porosity of 78%, a fine pore size of 112.8 μm, and a total pore volume of 7.0 cm3·g-1. The initial total thermal conductivity of the wood fiber VIP was 9.4 mW/(m·K) at 25 °C. The thermal conductivity of the VIP increased with increasing ambient temperature. These results were relatively good compared to the thermal insulation performance of current biomass VIPs, so the use of wood fiber as a VIP core material has broad application prospects.

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SAETRUM OPGAARD, Ole, Mikael KNUTSSON, René DE VRIES, Beril TOM, Pramod R. SAXENA, and Lars EDVINSSON. "Vasoactive intestinal peptide has a direct positive inotropic effect on isolated human myocardial trabeculae." Clinical Science 101, no. 6 (November 20, 2001): 637–43. http://dx.doi.org/10.1042/cs1010637.

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The aim of the present study was to assess the inotropic effects of vasoactive intestinal peptide (VIP) on isolated myocardial trabeculae from the right atrium and the left ventricle of human hearts. Furthermore, using reverse transcriptase-PCR, we wanted to determine the presence of mRNAs encoding the three cloned human VIP receptors, VPAC1, VPAC2 and PAC1. The trabeculae were paced at 1.0Hz in tissue baths, and changes in isometric contractile force upon exposure to agonist were studied. VIP had a potent positive inotropic effect in some of the atrial and ventricular trabeculae tested. This effect was almost completely blocked by the VIP-receptor antagonist VIP-(6-28). mRNAs encoding the human VPAC1, VPAC2 and PAC1 receptors were detected in human myocardial trabeculae from both the right atrium and the left ventricle. In conclusion, VIP has a direct positive inotropic effect in both the atria and the ventricles of the human heart. The presence of mRNAs for the VPAC1, VPAC2 and PAC1 receptors suggest that VIP may mediate its effect via these receptors.

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HILL, JOANNA M., RONALD F. MERVIS, JOEL POLITI, SUSAN K. McCUNE, ILLANA GOZES, MATI FRIDKIN, and DOUGLAS E. BRENNEMAN. "Blockade of VIP during Neonatal Development Induces Neuronal Damage and Increases VIP and VIP Receptors in Brain." Annals of the New York Academy of Sciences 739, no. 1 Models of Neu (October 1994): 211–25. http://dx.doi.org/10.1111/j.1749-6632.1994.tb19823.x.

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Hagen, Brian M., Orline Bayguinov, and Kenton M. Sanders. "VIP and PACAP regulate localized Ca2+ transients via cAMP-dependent mechanism." American Journal of Physiology-Cell Physiology 291, no. 2 (August 2006): C375—C385. http://dx.doi.org/10.1152/ajpcell.00495.2005.

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Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) have been suggested as participants in enteric inhibitory neural regulation of gastrointestinal motility. These peptides cause a variety of postjunctional responses including membrane hyperpolarization and inhibition of contraction. Neuropeptides released from enteric motor neurons can elicit responses by direct stimulation of smooth muscle cells as opposed to other transmitters that rely on synapses between motor nerve terminals and interstitial cells of Cajal. Therefore, we studied the responses of murine colonic smooth muscle cells to VIP and PACAP(1–38) with confocal microscopy and patch-clamp technique. Localized Ca2+ transients (Ca2+ puffs) were observed in colonic myocytes, and these events coupled to spontaneous transient outward currents (STOCs). VIP and PACAP increased Ca2+ transients and STOC frequency and amplitude. Application of dibutyryl cAMP had similar effects. The adenylyl cyclase blocker MDL-12,330A alone did not affect spontaneous Ca2+ puffs and STOCs but prevented responses to VIP. Disruption of A-kinase-anchoring protein (AKAP) associations by application of AKAP St-Ht31 inhibitory peptide had effects similar to those of MDL-12,330A. Inhibition of ryanodine receptor channels did not block spontaneous Ca2+ puffs and STOCs but prevented the effects of dibutyryl cAMP. These findings suggest that regulation of Ca2+ transients (which couple to activation of STOCs) may contribute to the inhibitory effects of VIP and PACAP. Regulation of Ca2+ transients by VIP and PACAP occurs via adenylyl cyclase, increased synthesis of cAMP, and PKA-dependent regulation of ryanodine receptor channels.

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Li, Jingxia, Reema Panjwani, Jian-Ming Li, Cynthia R. Giver, Maryellen Malone, and Edmund K. Waller. "T Cell Activation By Plasmacytoid Dendritic Cells Is Augmented By Inhibition of Vasoactive Intestinal Polypeptide Signaling: Implications for Cellular Immunotherapy." Blood 126, no. 23 (December 3, 2015): 3438. http://dx.doi.org/10.1182/blood.v126.23.3438.3438.

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Abstract Introduction: Data from clinical allogeneic bone marrow transplant (allo-BMT) and pre-clinical murine models of allo-BMT have shown that donor plasmacytoid dendritic cells (pDC) have important roles in regulating graft-versus-host disease (GvHD) and graft-versus-leukemia (GvL) activities of donor T cells. Using murine models of allo-BMT we have previously shown that 1) donor pDCs induce Th1 polarization of donor T cells and augment the GvL activity of T cells; and 2) the addition of pDC to grafts composed of purified T cells and HSC limited the subsequent development of GvHD. VIP is an immunosuppressive neuropeptide that regulates adaptive immune responses. We reasoned that VIP signaling may regulate activation of allo-specific T-cells, and the VIP pathway may be target for regulating GvHD and GvL in allo-BMT. Methods: To explore the mechanisms by which pDC and VIP signaling regulate T cell activation we used: 1) transgenic mice expressing GFP under the control of the VIP promoter to measure VIP expression in vivo in allo-BMT recipients; 2) one-way mixed lymphocyte reaction (MLR) to measure the proliferative response of transgenic luciferase positive T cells in response to allo-antigens via bioluminescence imaging (BLI); and 3) a model system of indirect presentation of allo-peptides derived from a H2-Ab MHC class II molecule by pDC to transgenic T cells expressing the TEa TCR. The effect of blocking vasoactive intestinal polypeptide (VIP) signaling during activation of allo-reactive T cells was assessed by using VIP-KO cells and by the addition of VIP peptide or a peptide antagonist of VIP (VIPhyb) to the one-way MLR. T cell proliferation and activation was measured by flow cytometry. Results: Analysis of VIP expression in donor pDC in murine models of allo-BMT showed >100-fold induction of VIP promoter activity in donor pDC and donor T cells during the first two weeks post-transplant, indicating that VIP expression in donor pDC may regulate T cell activation.Addition of endogenous native VIP suppressed T cell proliferation in one-way MLR but was reversed by addition of a 10x concentration of the VIP antagonist peptide (Figure 1B). Furthermore, adding 3 uM of the VIP antagonist to the MLR cultured significantly enhanced T cell proliferation. TEa peptide-primed T cells cultures with peptide-primed pDC from VIP knock-out mice had increased proliferation and expressed more of the activation markers CD69 and CD71 compared with T cells cultured with VIP-WT pDCs. Comparing pDC purified from marrow versus spleen, we found significantly more proliferation in T cells cultured with bone marrow VIP-KO pDCs than splenic VIP-KO pDCs, indicating that the less mature marrow pDC have greater antigen presenting ability than the more mature splenic pDC. Conclusion: These data suggest that 1) VIP is produced by donor pDC early after allo-BMT; 2) VIP inhibits T cell allo-proliferation in one-way MLR's; and 3) blocking VIP signaling using donor cells that cannot produce VIP or through the use of pharmacological inhibitors of VIP can augment activation and proliferation of T cells in response to indirect antigen presentation.The present findings support studies of VIP antagonist in allo-BMT to augment the GvL activity of T cells through indirect antigen presentation. Future studies include using the BLI analysis of MLR to determine the effect of novel drugs on T cell proliferation. **Jingxia Li and Reema Panjwani were equal contributors to this abstract. Disclosures No relevant conflicts of interest to declare.

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Algazi, M. C., H. S. Chen, M. A. Koss, D. L. Hogan, J. Steinbach, S. J. Pandol, and J. I. Isenberg. "Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 5 (May 1, 1989): G833—G836. http://dx.doi.org/10.1152/ajpgi.1989.256.5.g833.

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Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.

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Kurjak, M., A. Sennefelder, M. Aigner, V. Schusdziarra, and H. D. Allescher. "Characterizing voltage-dependent Ca2+ channels coupled to VIP release and NO synthesis in enteric synaptosomes." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 5 (November 1, 2002): G1027—G1034. http://dx.doi.org/10.1152/ajpgi.00400.2001.

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In enteric synaptosomes of the rat, the role of voltage-dependent Ca2+channels in K+-induced VIP release and nitric oxide (NO) synthesis was investigated. Basal VIP release was 39 ± 4 pg/mg, and cofactor-substituted NO synthase activity was 7.0 ± 0.8 fmol · mg−1 · min−1. K+ depolarization (65 mM) stimulated VIP release Ca2+ dependently (basal, 100%; K+, 172.2 ± 16.2%; P < 0.05, n = 5). K+-stimulated VIP release was reduced by blockers of the P-type (ω-agatoxin-IVA, 3 × 10−8 M) and N-type (ω-conotoxin-GVIA, 10−6 M) Ca2+ channels by ∼50 and 25%, respectively, but not by blockers of the L-type (isradipine, 10−8 M), Q-type (ω-conotoxin-MVIIC, 10−6 M), or T-type (Ni2+, 10−6 M) Ca2+ channels. In contrast, NO synthesis was suppressed by ω-agatoxin-IVA, ω-conotoxin-GVIA, and isradipine by ∼79, 70, and 70%, respectively, whereas Ni2+ and ω-conotoxin-MVIIC had no effect. These findings are suggestive of a coupling of depolarization-induced VIP release primarily to the P- and N-type Ca2+ channels, whereas NO synthesis is presumably dependent on Ca2+ influx not only via the P- and N- but also via the L-type Ca2+ channel. In contrast, none of the Ca2+ channel blockers affected VIP release evoked by exogenous NO, suggesting that NO induces VIP secretion by a different mechanism, presumably involving intracellular Ca2+ stores.

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Murthy, K. S., B. Q. Teng, J. G. Jin, and G. M. Makhlouf. "G protein-dependent activation of smooth muscle eNOS via natriuretic peptide clearance receptor." American Journal of Physiology-Cell Physiology 275, no. 6 (December 1, 1998): C1409—C1416. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1409.

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In gastrointestinal smooth muscle, the neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) induce relaxation by interacting with VIP2/PACAP3receptors coupled via Gs to adenylyl cyclase and with distinct receptors coupled via Gi1 and/or Gi2 to a smooth muscle endothelial nitric oxide synthase (eNOS). The present study identifies the receptor as the single-transmembrane natriuretic peptide clearance receptor (NPR-C). RT-PCR and Northern analysis demonstrated expression of the natriuretic peptide receptors NPR-C and NPR-B but not NPR-A in rabbit gastric muscle cells. In binding studies using125I-labeled atrial natriuretic peptide (125I-ANP) and125I-VIP as radioligands, VIP, ANP, and the selective NPR-C ligand cANP(4–23) bound with high affinity to NPR-C. ANP, cANP-(4–23), and VIP initiated identical signaling cascades consisting of Ca2+ influx, activation of eNOS via Gi1 and Gi2, stimulation of cGMP formation, and muscle relaxation. NOS activity and cGMP formation were abolished (93 ± 3 to 96 ± 2% inhibition) by nifedipine, pertussis toxin, the NOS inhibitor, N G-nitro-l-arginine, and the antagonists ANP-(1–11) and VIP-(10–28). NOS activity stimulated by all three ligands in muscle membranes was additively inhibited by Gi1 and Gi2 antibodies (82 ± 2 to 84 ± 1%). In reconstitution studies, VIP, cANP-(4–23), and guanosine 5′- O-(3-thiotriphosphate) stimulated NOS activity in membranes of COS-1 cells cotransfected with NPR-C and eNOS. The results establish a unique mechanism for G protein-dependent activation of a constitutive NOS expressed in gastrointestinal smooth muscle involving interaction of the relaxant neuropeptides VIP and PACAP with a single-transmembrane natriuretic peptide receptor, NPR-C.

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Lamouche, Stéphane, and Nobuharu Yamaguchi. "Role of PAC1 receptor in adrenal catecholamine secretion induced by PACAP and VIP in vivo." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (February 1, 2001): R510—R518. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r510.

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The present study was conducted to investigate the functional implication of the pituitary adenylate cyclase-activating polypeptide (PACAP) type I (PAC1) receptor in the adrenal catecholamine (CA) secretion induced by either PACAP-27 or vasoactive intestinal polypeptide (VIP) in anesthetized dogs. PACAP-27, VIP, and their respective antagonists were locally infused to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by means of a high-performance liquid chromatograph coupled with an electrochemical detector. Adrenal venous blood flow was measured by gravimetry. The administration of PACAP-27 (50 ng) resulted in a significant increase in adrenal CA output. VIP (5 μg) also increased the basal CA secretion to an extent comparable to that observed with PACAP-27. In the presence of PACAP partial sequence 6–27 [PACAP-(6–27); a PAC1 receptor antagonist] at the doses of 7.5 and 15 μg, the CA response to PACAP-27 was attenuated by ∼50 and ∼95%, respectively. Although the CA secretagogue effect of VIP was blocked by ∼85% in the presence of PACAP-(6–27) (15 μg), it remained unaffected by VIP partial sequence 10–28 [VIP-(10–28); a VIP receptor antagonist] at the dose of 15 μg. Furthermore, the CA response to PACAP-27 did not change in the presence of the same dose of VIP-(10–28). The results indicate that PACAP-(6–27) diminished, in a dose-dependent manner, the increase in adrenal CA secretion induced by PACAP-27. The results also indicate that the CA response to either PACAP-27 or VIP was selectively inhibited by PACAP-(6–27) but not by VIP-(10–28). It is concluded that PAC1receptor is primarily involved in the CA secretion induced by both PACAP-27 and VIP in the canine adrenal medulla in vivo.

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Journal articles on the topic 'VIP'

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