Journal articles: 'Muscle lisse'

1

Fattoum, A. "Régulation de la contraction du muscle lisse." médecine/sciences 13, no. 6-7 (1997): 777. http://dx.doi.org/10.4267/10608/462.

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Marthan, Roger. "Mécanismes cellulaires de la contraction du muscle lisse bronchique." Archives Internationales de Physiologie, de Biochimie et de Biophysique 100, no. 4 (January 1992): A27—A40. http://dx.doi.org/10.3109/13813459209000711.

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Jammes, Yves. "Le tonus du muscle lisse trachéobronchique et son controle réflexe." Archives Internationales de Physiologie et de Biochimie 97, no. 4 (January 1989): A15—A35. http://dx.doi.org/10.3109/13813458909105525.

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Marthan, R., and J. P. Savineau. "Physiologie cellulaire et pharmacologie moléculaire du muscle lisse des voies aériennes." Revue Française d'Allergologie et d'Immunologie Clinique 37, no. 4 (June 1997): 479–86. http://dx.doi.org/10.1016/s0335-7457(97)80079-2.

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Cortes, Diego, M. Yolanda Torrero, M. Pilar D'Ocon, M. Luz Candenas, André Cavé, and A. Hamid A. Hadi. "Norstephalagine et Atherospermidine, Deux Aporphines d'Artabotrys maingayi Relaxantes du Muscle Lisse." Journal of Natural Products 53, no. 2 (March 1990): 503–8. http://dx.doi.org/10.1021/np50068a039.

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Hadchouel, J., and S. Tajbakhsh. "La transdifférenciation du muscle lisse en muscle squelettique dans l'oesophage est dirigée par Myf5 et MyoD." médecine/sciences 16, no. 12 (2000): 1428. http://dx.doi.org/10.4267/10608/1601.

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Bégueret, H., P. Berger, P. O. Girodet, J. M. Vernejoux, R. Marthan, and J. M. Tunon de Lara. "070 Approche ultrastructurale de l’inflammation du muscle lisse bronchique dans l’asthme allergique." Revue des Maladies Respiratoires 22, no. 5 (November 2005): 880. http://dx.doi.org/10.1016/s0761-8425(05)92482-0.

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Siao, Valérie, and M. Fayon. "La cellule du muscle lisse et la mitochondrie dans l’asthme : Forever young." Revue des Maladies Respiratoires 31, no. 9 (November 2014): 885. http://dx.doi.org/10.1016/j.rmr.2014.06.027.

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Esteves, P., A. Celle, P. Berger, and T. Trian. "La mitochondrie du muscle lisse bronchique : une nouvelle cible thérapeutique dans l’asthme?" Revue des Maladies Respiratoires 37, no. 3 (March 2020): 201–4. http://dx.doi.org/10.1016/j.rmr.2020.02.004.

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Adnot, S., N. Frossard, S. Eddahibi, and E. Artaud-Macari. "Endothélium et muscle lisse dans le développement et la progression de l’HTAP." Revue des Maladies Respiratoires Actualités 3, no. 3 (November 2011): 213–17. http://dx.doi.org/10.1016/s1877-1203(11)70094-5.

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Rimbach, Gerald, Anne Marie Minihane, Jonathan Majewicz, Alexandra Fischer, Josef Pallauf, Fabio Virgli, and Peter D. Weinberg. "Regulation of cell signalling by vitamin E." Proceedings of the Nutrition Society 61, no. 4 (November 2002): 415–25. http://dx.doi.org/10.1079/pns2002183.

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RésuméLa vitamine E, l'antioxydant liposoluble le plus important, fut découverte à l'Université de Californie à Berkeley en 1922. Depuis sa découverte, les études sur les tocophérols et les tocotrienols que constitue cette vitamine, ont été centrées pour la plupart sur leurs propriétés antioxydantes. En 1991, le groupe de Angelo Azzi (Boscoboinik et al. 1991a,b) fut le premier à décrire les fonctions autres que les antioxydantes et de transmission de signaux de l'α-tocophérol, en démontrant la régulation par la vitamine E de l'activité de la protéine kinase C dans les cellules de muscle lisse. Au niveau de la transcription, l'²-tocophérol module l'expression de la protéine de transfert hépatique de l'α-tocophérol, ainsi que l'expression du ge`ne alpha1 du collage`ne du foie, du ge`ne de la collagénase et du ge`ne de l'α-tropomyosine. Récemment, un facteur de transcription dépendant du tocophérol (la protéine associée au tocophérol) a été découvert. Il a été démontré sur des cellules cultivées que la vitamine E inhibe l'inflammation, l'adhésion cellulaire, l'agrégation des plaquettes et la prolifération des cellules de muscle lisse. Les avancées récentes de la biologie moléculaire et des techniques génomiques ont conduit à la découverte de nouveaux ge`nes et des mécanismes de transduction des signaux sensibles à la vitamine E.

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Hamet, P., V. Hadrava, U. Kruppa, and J. Tremblay. "Facteurs de croissance et prolifération du muscle lisse vasculaire dans l'hypertension et le diabète." médecine/sciences 5, no. 9 (1989): 654. http://dx.doi.org/10.4267/10608/4040.

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Raison, D., C. Coquard, M. Hochane, T. Massfelder, B. Moulin, D. Metzger, J. J. Helwig, and M. Barthelmebs. "Effets hémodynamiques rénaux de la délétion conditionnelle CreLox en PTHrP dans le muscle lisse." Néphrologie & Thérapeutique 7, no. 5 (September 2011): 294. http://dx.doi.org/10.1016/j.nephro.2011.07.074.

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Quittelier, E., J. Buvat, A. Lemaire, M. Buvat-Herbaut, G. Marcolin, and JM Rigot. "L’electromyographie du penis: Une nouvelle exploration du muscle lisse caverneux et de son controle neurologique?" Andrologie 1, no. 3 (September 1991): 109–11. http://dx.doi.org/10.1007/bf03034262.

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Trian, T., P. O. Girodet, H. Begueret, O. Ousova, R. Marthan, J. M. Tunon de Lara, and P. Berger. "001 Rôle de la mitochondrie dans le remodelage du muscle lisse bronchique des patients asthmatiques sévères." Revue des Maladies Respiratoires 23, no. 5 (November 2006): 509. http://dx.doi.org/10.1016/s0761-8425(06)71829-0.

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Colombat, M., S. Pegorier, M. C. Dombret, M. Aubier, and M. Pretolani. "091 Caractérisation du phénotype du muscle lisse bronchique dans l’asthme sévère avec trouble ventilatoire obstructif (TVO) fixé." Revue des Maladies Respiratoires 22, no. 5 (November 2005): 891. http://dx.doi.org/10.1016/s0761-8425(05)92503-5.

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Colombat, M., and M. Pretolani. "24 Antadir Etude des anomalies du muscle lisse bronchique associées au trouble ventilatoire obstructif fixé dans l’asthme." Revue des Maladies Respiratoires 21, no. 2 (April 2004): 437. http://dx.doi.org/10.1016/s0761-8425(04)71336-4.

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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en microscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A328—A329. http://dx.doi.org/10.1016/j.rmr.2016.10.868.

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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en miscroscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A26—A27. http://dx.doi.org/10.1016/j.rmr.2016.10.056.

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Mbikou, P., A. Ajmut, M. Brumen, and E. Roux. "015 Étude expérimentale et théorique du rôle de la Rhokinase dans la contraction du muscle lisse des voies aériennes." Revue des Maladies Respiratoires 24, no. 9 (November 2007): 1195. http://dx.doi.org/10.1016/s0761-8425(07)74306-1.

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Forestier, F., E. Roux, G. Janvier, and R. M.A.rthan. "R520 Effets inhibiteurs du propofol et de l'étomidate sur la signalisation calcique du muscle lisse des voies aériennes normales et pathologiques." Annales Françaises d'Anesthésie et de Réanimation 17, no. 8 (January 1998): 1071. http://dx.doi.org/10.1016/s0750-7658(98)80638-2.

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22

Gazzola, M., N. Flamand, and Y. Bossé. "La contractilité du muscle lisse des voies respiratoires est régulée par de nombreuses molécules extracellulaires qui pourraient contribuer à l’hyperréactivité bronchique." Revue des Maladies Respiratoires 37, no. 6 (June 2020): 462–73. http://dx.doi.org/10.1016/j.rmr.2020.03.009.

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23

Nowell, W. B., K. Gavigan, T. Hunter, W. Malatestinic, R. Bolce, J. Lisse, C. Himelein, J. Curtis, and J. A. Walsh. "POS1499-PARE PATIENT PERSPECTIVES OF BIOLOGIC TREATMENTS FOR AXIAL SPONDYLOARTHRITIS: SATISFACTION, WEAR-OFF BETWEEN DOSES, AND USE OF SUPPLEMENTAL MEDICATIONS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1034–35. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1876.

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Background:Biologic disease-modifying antirheumatic drug (bDMARD) therapy has been shown to be effective in the treatment of axial spondyloarthritis (axSpA).1,2 Little is understood about patients’ experience of axSpA treatment from their own perspective.Objectives:To characterize patient experiences and perspectives with bDMARD treatments for axSpA, including satisfaction, and use of supplementary treatments when wear-off between doses is perceived among those currently treated with bDMARD therapy.Methods:Adult US participants (pts) within the ArthritisPower registry with physician-diagnosed axSpA were invited to complete electronic PRO measures, such as the BASDAI (0-10 scale, score ≥4 indicates suboptimal disease control), and an online survey about their perspectives of treatment. Analysis compared pt characteristics and treatment satisfaction by whether or not pt reported wear-off between bDMARD doses.Results:128 pts with axSpA and on bDMARD therapy met inclusion criteria of whom 82.8% were female, with mean age of 47 years. Mean BASDAI scores indicated poor disease control (6.4, SD 1.8), worse for those perceiving wear-off between doses compared with those who did not [6.8 (1.6) vs. 5.9 (2.0), p=0.01]. A majority of pts on a bDMARD reported being somewhat (57.8%) or very satisfied (26.6%) with their current axSpA treatment, and about 53.1% were satisfied with how well it controls axSpA-related pain. However, 60.9% (n=78) of pts reported that their current bDMARD typically wears off before the next dose. Treatment satisfaction was lower for pts experiencing wear-off compared to pts without wear-off (highly satisfied: 21.8% vs. 34%; somewhat satisfied: 60.3% vs. 54%; dissatisfied: 17.9% vs. 12%). 82.1% (n=64) of pts reporting wear-off used additional medications or supplements when that happened, chiefly NSAIDs (68.8%, n=44), muscle relaxers (42.2%, n=27) and/or opioids (37.5%, n=24). Among the 20 pts not satisfied with current axSpA treatment, side effects (6/20, 30.0%), or worry about risk of side effects (2/20, 10%) were the main reasons.Conclusion:In a predominantly female sample of bDMARD-treated axSpA patients with high disease activity, most expressed satisfaction with treatment. However, most experienced wear-off between doses and took supplementary medications, including opioids, to manage.References:[1]Dubash S, et al. Ther Adv Chronic Dis. 2018;9(3):77–8.[2]Van Der Heijde D, et al. Ann Rheum Dis. 2017;76(6):978–91.Table 1.Demographic and clinical characteristics by wear-off between bDMARD doses (n=128)Pts currently on bDMARD(N=128)Wear-off between bDMARD oses(N=78)No wear-off / Not sure(N=50)p-valueNumber or mean (% or SD)Age46.9 (10.3)46.1 (9.2)48.2 (11.8)0.25Female106 (82.8)69 (88.5)37(74.0)0.03White115 (89.8)70 (89.7)45 (90.0)0.96Body Mass Index30.9 (7.8)31.2 (8.5)30.4 (6.6)0.57Current Medications, addition to bDMARDConventional Synthetic DMARD (e.g. methotrexate, sulfasalazine)17 (13.3)15 (19.2)2 (4.0)0.01Prescription NSAID59 (46.1)39 (50.0)20 (40.0)0.27Other prescription medication¥70 (54.7)44 (56.4)26 (52.0)0.62Noticed improvement in symptoms related to axSpA since starting current bDMARD80 (62.5)51 (65.4)29 (58.0)0.40Noticed improvement in symptoms NOT related to axSpA since starting current bDMARD40 (31.3)22 (28.2)18 (36.0)0.35BASDAI‡6.4 (1.8)6.8 (1.6)5.9 (2.0)0.01PROMIS Pain Interference ł65.3 (5.7)66.0 (5.1)64.3 (6.4)0.09PROMIS Physical Function ł36.7 (5.6)36.1 (5.3)37.7 (5.8)0.11PROMIS Sleep Disturbance ł59.8 (8.5)61.2 (7.7)57.6 (9.3)0.02* Statistical significance between groups of pts who experienced wear-off between bDMARD or not, p < 0.05¥ Other prescription medications: muscle relaxers, nerve pain medications or anti-depressants, and opioids‡ BASDAI is scored on a 0-10 scale with score ≥4 indicating suboptimal control of diseaseł PROMIS measures use T-score metric in which 50 is mean, 10 is standard deviation (SD), of US population; higher T-score = more of concept measuredAcknowledgements:This study was sponsored by Eli Lilly and Company. We thank the patients who participated in this study.Disclosure of Interests:W. Benjamin Nowell Grant/research support from: Full-time employee of Global Healthy Living Foundation, an independent nonprofit research organization, which received funding pursuant to a contract from Eli Lilly to conduct the study that is the subject of this abstract; Principal Investigator for studies with grant support from AbbVie, Amgen and Eli Lilly, Kelly Gavigan Grant/research support from: Full-time employee of Global Healthy Living Foundation, an independent nonprofit research organization, which received funding pursuant to a contract from Eli Lilly to conduct the study that is the subject of this abstract, Theresa Hunter Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, William Malatestinic Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Rebecca Bolce Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Jeffrey Lisse Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Carol Himelein Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Jeffrey Curtis Consultant of: AbbVie, Amgen, BMS, Corrona, Eli Lilly, Janssen, Myriad, Pfizer, Roche, Regeneron, Radius, UCB, Grant/research support from: AbbVie, Amgen, BMS, Corrona, Eli Lilly, Janssen, Myriad, Pfizer, Roche, Regeneron, Radius, UCB, Jessica A. Walsh Consultant of: AbbVie, Amgen, Eli Lilly and Company, Janssen, Merck, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Merck, Pfizer

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Loirand, G., AM Lompré, JP Savineau, and P. Pacaud. "Tonus des muscles lisses vasculaires : translissions du signal dépendantes et indépendantes du Ca2+." médecine/sciences 13, no. 6-7 (1997): 766. http://dx.doi.org/10.4267/10608/461.

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Saneto, Russell P. "The pharmacology of nerve and muscle in tissue culture. Alan L. Harvey, Alan R. Liss, Inc., New York, 1984." Journal of Neuroscience Research 13, no. 3 (1985): 461–62. http://dx.doi.org/10.1002/jnr.490130312.

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Khaddaj-Mallat, R., R. Hiram, Y. Tabet, and E. Rousseau. "Le 17(18)-EpETE, un époxy-eicosanoïde dérivé de l’EPA, diminue l’hyperréactivité des muscles lisses des voies respiratoires." Revue des Maladies Respiratoires 31, no. 7 (September 2014): 647. http://dx.doi.org/10.1016/j.rmr.2014.04.006.

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Khaddaj-Mallat, R., C. Sirois, M. Sirois, E. Rizcallah, and E. Rousseau. "La Résolvine D1 diminue l’inflammation et la sensibilité au Ca2+ des muscles lisses des bronchioles humaines prétraitées à l’interleukine 13." Revue des Maladies Respiratoires 32, no. 3 (March 2015): 314. http://dx.doi.org/10.1016/j.rmr.2015.02.028.

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Schanck, A., and F. Baguet. "Application de la Technique RMN de Transfert de Saturation Pour Mesurer L'Activité Enzymatique dans des Muscles Lisses de Mytilus Edulis." Bulletin des Sociétés Chimiques Belges 97, no. 11-12 (September 1, 2010): 977–82. http://dx.doi.org/10.1002/bscb.19880971123.

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Goldman, Steven A. "The pharmacology of nerve and muscle in tissue culture. By Alan L. Harvey, New York, Alan R. Liss, 1984, 260 pp, illustrated, $48.00." Annals of Neurology 17, no. 4 (April 1985): 420. http://dx.doi.org/10.1002/ana.410170426.

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Whitelaw, W. "RESPIRATORY MUSCLES AND THEIR NEUROMOTOR CONTROL. Edited by G.C. Sieck, S.G. Gandevia, W.E. Cameron. Published by Alan R. Liss Inc., New York, 1987." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 15, no. 2 (May 1988): 169. http://dx.doi.org/10.1017/s0317167100027591.

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Vervullens, S., L. Meert, I. Baert, N. Delrue, K. Heusdens, A. Hallemans, T. Van Criekinge, R. Smeets, and K. De Meulemeester. "POS1096 THE EFFECT OF ONE DRY NEEDLING SESSION ON PAIN AND CENTRAL PAIN PROCESSING IN PATIENTS WITH KNEE OSTEOARTHRITIS: A RANDOMIZED CONTROLLED TRIAL." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 828.1–828. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2108.

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Background:Osteoarthritis (OA) is the leading cause of chronic disability in the elderly1,2. Abnormal central pain processing (CPP) is present in around 30% of the knee OA patients3 and can be partly induced by peripheral nociception through long term potentiation4. An attempt to resolve abnormal CPP can be to eliminate this nociception5. Myofascial trigger points (MTrPs) are often present in knee OA6, can lead to nociception7 and therefore abnormal CPP if prolonged present8. These are usually defined as hypersensitive tender spots within taut bands of a muscle9. Additionally, both MTrPs and knee OA can induce disturbed motor control, increased co-antagonist activation and modified gait pattern10,11. Dry needling (DN) is often used to deactivate the MTrP and thus resolve the source of nociception, which normally results in reducing pain and restoring muscle dysfunction12. However, studies about the effect of DN on CPP and other outcomes than pain are very limiting. Therefore, more high-quality studies concerning DN and its effects on CPP, muscle features and gait are needed13,14.Objectives:The aim of this randomized controlled trial is to assess the effect of one DN session compared to one sham needling (SN) session on pain (processing), muscle activity and gait in patients with knee OA.Methods:61 patients participated of which 31 were allocated to the DN and 30 to the SN group. Each patient underwent one treatment session. Primary outcomes were pain intensity, measured with questionnaires; and CPP, measured with quantitative sensory testing. Secondary outcomes included muscle co-activation, measured with electromyography; and spatiotemporal parameters, measured with gait analysis. Patients were assessed at baseline, 15 minutes (post 1) and 3 days after intervention (post2- only for the outcome pain). Linear mixed models was used to identify the possible differences over time between the two therapy modalities.Results:The following significant within group differences were observed: decreased pain, stride- and step time and increased widespread pain pressure threshold and step length. A significant between group difference of the conditioned pain modulation score was found, whereas the SN group showed a decrease in difference between the pain pressure threshold scores (with and without conditioning stimulus) and the DN group remained stable. No other significant between or within group differences were detected. However, if we compared both interventions, the change over time for the visual analogue scale (VAS) behaved different in the DN (p<0.05, post 2 - baseline) and SN group (p<0.05, post 1 - baseline and post 2 - post 1).Conclusion:One DN session has no larger effect on all outcome measurements compared to SN. Both therapies seem to be useful to improve pain and widespread pain pressure threshold in short term, however the improvement of pain differs in the groups. Although improvements in some spatiotemporal parameters were observed, it is uncertain they are of clinical relevance or related to treatment. More research is necessary to reveal the ideal number of sessions of DN to improve outcomes and to reveal the effect of DN compared to no treatment, as SN could have hide the real treatment effect.References:[1]Reginster, J. Y. Rheumatol. Oxf. 41 Supp 1, 3–6 (2002)[2]Lespasio, M. J. et al. Perm J 21, 16–183 (2017)[3]Lluch, E. et al. Eur J Pain 18, 1367–75 (2014)[4]Mease, P. J. et al. J. Rheumatol. 38, 1546–1551 (2011)[5]Nijs, J. et al. Expert Opin Pharmacother 15, 1671–83 (2014)[6]Bajaj, P. et al. J. Musculoskelet. Pain 9, 17–33 (2001)[7]Jafri, M. S. Int. Sch. Res. Not. 2014, (2014)[8]Cagnie, B. et al. Curr Pain Headache Rep 17, 348 (2013)[9]Borg-Stein, J. et al. Arch. Phys. Med. Rehabil. 83, S40–S47 (2002)[10]Childs, J. D. et al. Clin. Biomech. 19, 44–9 (2004)[11]Ibarra, J. M. et al. J Pain 12, 1282–8 (2011)[12]Rahou-El-Bachiri, Y. et al. J. Clin. Med. 9, (2020)[13]Stieven, F. F. et al. J. Manipulative Physiol. Ther. (2021)[14]Dor, A. et al. J Bodyw Mov Ther 21, 642–647 (2017)Figure 1.Mean and standard error of VAS scores over time in the DN and SN groupAcknowledgements:I like to thank and acknowledge the contribution of the other executive researchers (Lise Brosens, Ayoub El Bouchaoni, Ben Ceusters, Sven Huybrechts and Mathias Van Loon), the participated dry needling therapists, Dry Needling Ghent, Trigger and the University Hospital of Antwerp.Disclosure of Interests:None declared.

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Mccaig, D. J. "Frontiers in Smooth Muscle Research, volume 327 inProgress in Clinical and BiologicalResearch. Edited by N.Sperelakisand J.D.Wood. Wiley-Liss, New York, 1989.$195.00 hardback. ISBN 0-471-56683-7." Experimental Physiology 76, no. 2 (March 1, 1991): 305. http://dx.doi.org/10.1113/expphysiol.1998.sp004190.

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Cherniack, Neil S. "Respiratory muscles and their neuromotor control. Edited by Gary C. Sieck, Simon C. Gandevia and William E. Cameron. Alan R. Liss, Inc., New York, 1987." Synapse 2, no. 3 (1988): 336–37. http://dx.doi.org/10.1002/syn.890020327.

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Hou-Dong, Li, Shu Bin, Xu Ying-Bin, Shi Yan, Qi Shao-Hai, Li Tian-Zeng, Liu Xu-Sheng, Tang Jin-Ming, and Xie Ju-Lin. "Differentiation of Rat Dermal Papilla Cells into Fibroblast-Like Cells Induced by Transforming Growth Factor β1." Journal of Cutaneous Medicine and Surgery 16, no. 6 (November 2012): 400–406. http://dx.doi.org/10.1177/120347541201600608.

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Background: The origin of wound-healing fibroblasts is still debated. Dermal papilla cells (DPCs), which are an important population of stem cells for the regeneration of hair follicles, play a considerable role in cutaneous wound healing. Based on the plasticity of DPCs in wound healing, we hypothesized that DPCs may contribute to the fibroblast population of wound repair. Objective: To explore the possibility of differentiation of DPCs into fibroblasts induced by transforming growth factor β1 (TGF-β1). Methods: The fourth passage DPCs were treated with TGF-β1 (10 ng/mL) for 4 days, and a series of methods was used to observe morphologic changes under an inverted phase contrast microscope, to validate the messenger ribonucleic acid expression change in α-smooth muscle actin (α-SMA) and vimentin by quantitative real-time reverse transcriptase polymerase chain reaction (QRT-PCR), to analyze the expression of α-SMA and vimentin protein by flow cytometry, and to semiquantitatively measure the expression of fibroblast-specific protein 1 (FSP1) by Western blot. Results: DPCs treated with TGF-β1 presented fibroblast-like changes in morphology and immunocytochemistry. The effects of TGF-β1 on α-SMA and vimentin in DPCs were detected on both the transcriptional and the posttranscriptional levels. The results showed that TGF-β1 significantly downregulated α-SMA expression and enhanced the expression of vimentin at all times tested. Further study revealed that TGF-β1 could gradually promote the expression of FSP1 in a time-dependent manner. Conclusion: DPCs experienced the changes in molecular marker expression in response to TGF-β1, which may be a key source of fibroblasts in wound healing. Contexte: L'origine des fibroblastes dans la cicatrisation fait encore l'objet de débats. Les cellules des papilles dermiques (CPD), qui constituent une population importante de cellules souches pour la régénération des follicules pileux, jouent un rôle considérable dans la cicatrisation du tissu cutané. Compte tenu de la plasticité des CPD dans la cicatrisation, nous avons émis l'hypothèse selon laquelle les CPD pourraient contribuer à l'accroissement de la population de fibroblastes dans la cicatrisation. Objectif: L'étude visait à examiner la possibilité de différenciation des CPD en fibroblastes, provoquée par le facteur de croissance transformant β1 (TGF-β1). Méthodes: Les CPD ont été traités, au quatrième passage, au TGF-β1 (10 ng/mL), pendant 4 jours, et nous avons eu recours à la microscopie à contraste de phase inversée pour observer les changements morphologiques; à la réaction en chaîne par polymérase quantitative, en temps réel, après transcription inverse (RCP-TI) pour valider le changement d'expression de l'acide ribonucléique messager de l'actine des muscles lisses alpha (AMC-α) et de la vimentine; à la cytométrie de flux pour analyser l'expression des protéines d'AMC-α et de vimentine; et au buvardage de Western pour obtenir une mesure semiquantitative de l'expression de la protéine 1 spécifique des fibroblastes (PSF1). Résultats: Les CPD traités au TGF-β1 ont subi des changements morphologiques et immunocytochimiques leur conférant un caractère fibroblastoïde. Les effets du TGF-β1 sur l'AMC-α et la vimentine dans les CPD ont été détectés aux phases transcriptionnelle et posttranscriptionnelle. D'après les résultats obtenus, le TGF-β1 a sensiblement régulé à la baisse l'expression de l'AMC-α et intensifié l'expression de la vimentine, et ce, à tous les points de vérification dans le temps. Enfin, une étude complémentaire a révélé que le TGF-β1 pouvait favoriser graduellement l'expression de la PSF1 en fonction du temps. Conclusion: Les CPD ont subi des changements tels d'expression de marqueurs moléculaires, en réaction au TGF-β1, qu'ils pourraient être une source importante de fibroblastes dans la cicatrisation.

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Risch, Lorenz, Tom Schleis, Katja Matozan, Benjamin Sakem, and Urs Nydegger. "Anti-A/B and Free Light Chains Kappa and Lambda: Components In Intravenous Immunoglobulin Preparations." Blood 116, no. 21 (November 19, 2010): 4404. http://dx.doi.org/10.1182/blood.v116.21.4404.4404.

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Abstract Abstract 4404 Hemolytic anemia and renal failure are among the very rare side effects related to immunoglobulin transfusions. Anti-A/B antibodies are implicated in hemolytic events upon transfusion of high doses, given in short time. Recently several cases of IVIG induced hemolytic anemia have been published as case reports (MJ Thomas et al. Blood 1993; AG Brox et al. Am J Med 1987; Z Daw et al. Transfusion 2008; JR Wilson et al. Muscle Nerve 1997; J Coghill et al. Biol Blood Marrow Transplant 2006; RL Comenzo et al. J Pediatr 1992; F Yin et al. J Hematol 2008). One recent report describes the development of acute kidney injury related to hemoglobinuria as a result of IVIG induced hemolytic anemia (CC Welles et al. Am J Kid Dis 2009). In most cases, high cumulative doses 2gr/kg were administered. Most of the patients showed a positive direct antiglobulin test, and most were of non-O blood type. Various concentrations of anti-A, anti-B, and anti-D hemagglutinin were detected in the different IVIG products that were infused in each case. A systematic comparison of anti A/B and free-light chain content was performed in 5 different, commercially available IVIG preparations. The quantitative estimation of IgG anti-A/B in IVIG preparations is depending on choosing the appropriate method. Thus, hemagglutination, ABO-ELISA, and FACS all detect some form of anti-A/B albeit with different sensitivity and specificity. The immune complex which forms in A1-patients will activate complement and induce the IVIG-associated hemolytic anemia. In such patients the Direct Antiglobulin Test (Coombs Test) will turn reactive. In most countries, health authorities set a limit of anti-A RBC agglutination titers <32 or <64 which is arbitrary of this semi quantitative procedure. Here we subject a hemagglutination system to various cell suspension buffer conditions and look at variations. To achieve high sensitivity in the hemagglutination striking-pattern assay, two type A1 red blood cells (RBC) were selected and the assay performed using 4 different suspension conditions as a function of pH and molarity. Quantitative estimation of light chains was done using nephelometry with polyclonal antibodies against the hidden light chain determinant on free kappa and lambda light chains devoid of cross-reaction with the kappa and lambda epitopes on intact IgG (The Binding Site, Oxford). A BN prospect system was used to evaluate the information. To determine the anti-A/B content a series of dilutions was made and the last agglutinating concentration (mg/(ml) was taken as the final content. The last agglutinating concentration of immunoglobulin preparations 1 to 5 varied from 1.95 to 25 in NaCl. In NaCl+Liss (low ionic strength solution, which enhances antigen-antibody binding) variation was from 6.25 to 25, in phosphate buffered saline (PBS) it varied from 4.4 to 25 and in PBS+Liss it varied from 3.125 to 25. Preparation 2 was the strongest agglutinator and preparation 4 the lowest in all milieus. The 5 IgG preparations assessed contained < 0.3% free kappa of total IgG and < 0.28% free lambda light chains. It is likely that the induction of side effects under usual administration conditions by anti-A is improbable with trigger limits acknowledged by the health authorities; however, transfusions of high doses of IVIG during short times could reach critical limits. High anti-A content IVIG transfusions, especially to A-type recipients, could reach critical limits to cause hemolysis. The FLC content appears at trace concentrations. References on poster Disclosures: Schleis: octapharma USA Inc: Employment. Nydegger:octapharma AG: Consultancy.

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Brading, A. F. "Regulation and Contraction of Smooth Muscle. (Proceedings of an IUPS satellite conference, Minaki, Ontario, Canada, July 1986.) Edited by M. J. Siegman, A. P. Somlyo & N. L. Stephens. Pp. 526. (Alan R. Liss, 1987.) $96.00." Quarterly Journal of Experimental Physiology 73, no. 3 (May 16, 1988): 456–57. http://dx.doi.org/10.1113/expphysiol.1988.sp003164.

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"Heterogeneity of airway smooth muscle / Hétérogénéité du muscle lisse des voies aériennes." Canadian Journal of Physiology and Pharmacology 75, no. 7 (July 1, 1997): 859. http://dx.doi.org/10.1139/cjpp75-7p859.

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Marthan, Roger. "Ozone et réactivité bronchique : effet sur le muscle lisse des voies aériennes." Pollution atmosphérique, N°142 (1994). http://dx.doi.org/10.4267/pollution-atmospherique.4136.

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"Models of smooth muscle contraction / Modèles de contraction des muscles lisses." Canadian Journal of Physiology and Pharmacology 83, no. 10 (October 1, 2005): iii. http://dx.doi.org/10.1139/y05-908.

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"Current understanding and issues in smooth muscle research: a tribute to Ed Daniel's contributions / État des connaissances et questions actuelles à propos de la recherche sur les muscles lisses : Hommage aux contributions d'Ed Daniel." Canadian Journal of Physiology and Pharmacology 83, no. 8-9 (August 1, 2005): iii—iv. http://dx.doi.org/10.1139/y05-905.

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Journal articles on the topic 'Muscle lisse'

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