Journal articles: 'Support prevents'

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Leahy, T., J. P. Rickard, R. J. Aitken, and S. P. de Graaf. "Penicillamine prevents ram sperm agglutination in media that support capacitation." REPRODUCTION 151, no. 2 (February 2016): 167–77. http://dx.doi.org/10.1530/rep-15-0413.

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Ram spermatozoa are difficult to capacitate in vitro. Here we describe a further complication, the unreported phenomenon of head-to-head agglutination of ram spermatozoa following dilution in the capacitation medium Tyrodes plus albumin, lactate and pyruvate (TALP). Sperm agglutination is immediate, specific and persistent and is not associated with a loss of motility. Agglutination impedes in vitro sperm handling and analysis. So the objectives of this study were to investigate the cause of sperm agglutination and potential agents which may reduce agglutination. The percentage of non-agglutinated, motile spermatozoa increased when bicarbonate was omitted from complete TALP suggesting that bicarbonate ions stimulate the agglutination process. d-penicillamine (PEN), a nucleophilic thiol, was highly effective at reducing agglutination. The inclusion of 250 μM PEN in TALP reduced the incidence of motile, agglutinated spermatozoa from 76.7±2.7% to 2.8±1.4%. It was then assessed if PEN (1 mM) could be included in existing ram sperm capacitation protocols (TALP +1 mM dibutyryl cAMP, caffeine and theophylline) to produce spermatozoa that were simultaneously capacitated and non-agglutinated. This protocol resulted in a sperm population which displayed high levels of tyrosine phosphorylated proteins and lipid disordered membranes (merocyanine-540) while remaining motile, viable, acrosome-intact and non-agglutinated. In summary, PEN (1 mM) can be included in ram sperm capacitation protocols to reduce sperm agglutination and allow for the in vitro assessment of ram sperm capacitation.

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Jung, Boris, Jean-Michel Constantin, Nans Rossel, Charlotte Le Goff, Mustapha Sebbane, Yannael Coisel, Gerald Chanques, et al. "Adaptive Support Ventilation Prevents Ventilator-induced Diaphragmatic Dysfunction in Piglet." Anesthesiology 112, no. 6 (June 1, 2010): 1435–43. http://dx.doi.org/10.1097/aln.0b013e3181d7b036.

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Background Contrary to adaptive support ventilation (ASV), prolonged totally controlled mechanical ventilation (CMV) results in the absence of diaphragm activity and causes ventilator-induced diaphragmatic dysfunction. Because maintaining respiratory muscles at rest is likely a major cause of ventilator-induced diaphragmatic dysfunction, ASV may prevent its occurrence in comparison with CMV. The aim of our study was to compare the effects of ASV with those of CMV on both in vivo and in vitro diaphragmatic properties. Methods Two groups of six anesthetized piglets were ventilated during a 72-h period. Piglets in the CMV group (n = 6) were ventilated without spontaneous ventilation, and piglets in the ASV group (n = 6) were ventilated with spontaneous breaths. Transdiaphragmatic pressure was measured after bilateral, supramaximal transjugular stimulation of the two phrenic nerves. A pressure-frequency curve was drawn after stimulation from 20 to 120 Hz of the phrenic nerves. Diaphragm fiber proportions and mean sectional area were evaluated. Results After 72 h of ventilation, transdiaphragmatic pressure decreased by 30% of its baseline value in the CMV group, whereas it did not decrease in the ASV group. Although CMV was associated with an atrophy of the diaphragm (evaluated by mean cross-sectional area of both the slow and fast myosin chains), atrophy was not detected in the ASV group. Conclusion Maintaining diaphragmatic contractile activity by using the ASV mode may protect the diaphragm against the deleterious effect of prolonged CMV, as demonstrated both in vitro and in vivo, in healthy piglets.

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Gohean, Jeffrey R., Erik R. Larson, Raul G. Longoria, Mark Kurusz, and Richard W. Smalling. "Preload Sensitivity with TORVAD Counterpulse Support Prevents Suction and Overpumping." Cardiovascular Engineering and Technology 10, no. 3 (June 11, 2019): 520–30. http://dx.doi.org/10.1007/s13239-019-00419-0.

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Brochard, Laurent, Alain Harf, Hubert Lorino, and François Lemaire. "Inspiratory Pressure Support Prevents Diaphragmatic Fatigue during Weaning from Mechanical Ventilation." American Review of Respiratory Disease 139, no. 2 (February 1989): 513–21. http://dx.doi.org/10.1164/ajrccm/139.2.513.

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Sanborn, Warren G. "Inspiratory Pressure Support Prevents Diaphragmatic Fatigue During Weaning from Mechanical Ventilation." American Review of Respiratory Disease 140, no. 3 (September 1989): 854. http://dx.doi.org/10.1164/ajrccm/140.3.854a.

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Gorlitzer, Michael, Sandra Folkmann, Johann Meinhart, Peter Poslussny, Markus Thalmann, Gabriel Weiss, Manfred Bijak, and Martin Grabenwoeger. "A newly designed thorax support vest prevents sternum instability after median sternotomy☆." European Journal of Cardio-Thoracic Surgery 36, no. 2 (August 2009): 335–39. http://dx.doi.org/10.1016/j.ejcts.2009.01.038.

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Jung, B., N. Rossel, C. Le Goff, N. Claveiras, M. Wysocki, S. Matecki, G. Chanques, and S. Jaber. "Adaptive support ventilation prevents ventilator-induced diaphragmatic dysfunction: an in vivo piglet study." Critical Care 13, Suppl 1 (2009): P31. http://dx.doi.org/10.1186/cc7195.

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Nong, Lingbo, Weibo Liang, Yuheng Yu, Yin Xi, Dongdong Liu, Jie Zhang, Jing Zhou, et al. "Noninvasive ventilation support during fiberoptic bronchoscopy-guided nasotracheal intubation effectively prevents severe hypoxemia." Journal of Critical Care 56 (April 2020): 12–17. http://dx.doi.org/10.1016/j.jcrc.2019.10.017.

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Harrison, Matthew W., and Amanda Young. "Noninvasive ventilation support during fiberoptic bronchoscopy-guided nasotracheal intubation effectively prevents severe hypoxemia." Journal of Emergency Medicine 58, no. 6 (June 2020): 982–83. http://dx.doi.org/10.1016/j.jemermed.2020.05.030.

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MIYAZAWA, KAZUTOSHI. "Old age support in kind." Journal of Pension Economics and Finance 9, no. 3 (July 21, 2009): 445–72. http://dx.doi.org/10.1017/s1474747209990096.

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AbstractIt has been argued whether a transfer policy for elderly people should be in kind or in cash. This paper presents a rationale to answer the question in an endogenous growth model with a two-way intrafamily transfer in middle age, education for the child as an inter-vivos transfer, and informal parental care in exchange for a bequest. We have two analytical results. First, a transfer in cash, such as a public pension, prevents economic growth because a strategic behavior concerning caregiving generates a disincentive effect on education. Second, a transfer in kind, such as public formal care, promotes economic growth because the valuation of the service generates an additional benefit of education, which dominates the disincentive effect. Our results show that old age support should be in kind rather than in cash in the context of economic growth and also welfare if bequests are strategic.

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Wang, Xiangdong, Gary C. Kanel, and Laurie D. DeLeve. "Support of sinusoidal endothelial cell glutathione prevents hepatic veno-occlusive disease in the rat." Hepatology 31, no. 2 (February 2000): 428–34. http://dx.doi.org/10.1002/hep.510310224.

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Lina, A. A., P. J. Dauchot, A. H. Anton, and R. Jezeski. "A845 IMMEDIATE VENTILATORY SUPPORT AFTER BUPIVACAINE-INDUCED APNEA PREVENTS CV COLLAPSE IN ANESTHETIZED RATS." Anesthesiology 73, no. 3A (September 1, 1990): NA. http://dx.doi.org/10.1097/00000542-199009001-00843.

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Novak-Marcincin, Jozef, Jozef Barna, and Jozef Torok. "Precision Assembly Process with Augmented Reality Technology Support." Key Engineering Materials 581 (October 2013): 106–11. http://dx.doi.org/10.4028/www.scientific.net/kem.581.106.

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This article presents possibilities of precision assembling process by using special tools of the augmented reality (AR) and logical procedures from related areas such as a Computer Aided Design and Planning. These possibilities are implemented in the virtual assembling environment of AR, where engineers and designers can see important information about an exact position and orientation of the single assembly element that creates a part of the entire assembly structure. By means of this the application of AR allows costumer to see the motion process of single assembly item according to its trajectory and prevents the possible mistakes in the assembling processes.

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Mianowana, Violetta, Marta Czekirda, Anna Bednarek, Dorota Nalepa, and Kinga Mianowana. "Expectations of patients for the support and the support for hemodialysis patients given by nurses." Pielegniarstwo XXI wieku / Nursing in the 21st Century 15, no. 1 (March 1, 2016): 16–21. http://dx.doi.org/10.1515/pielxxiw-2016-0003.

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AbstractIntroduction. Undoubtedly, the renal replacement therapy is stressful situation for the patients with chronic renal failure. Chronic disease limits and prevents meeting the psychosocial needs. It often causes the frustration, to which patients react in different ways.Aim of the Study. Purpose of the research was to investigate patients’ expectations for the support and to define the support given by nurses.Material and Methodology. One hyndred chronic renal failure patients were examined on the basis of an author’s questionnaire survey. Results were subjected to statistical analysis. Homogeneity test was used for unrelated quality characteristics to detect the existence of differences between compared groups.Results. Most of patients expected the support first from their families (39%), next from doctors and nurses. Almost everybody (95.0%) Experienced emotional support from nurses during every hemodialysis.Conclusions. The research shows that patients during stress expect a conversation and almost all of them accept the attitude of empathy. Those who received information support felt less stressed.

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Yi, Se Won, Young Min Shin, Jung Bok Lee, Ju Young Park, Dae‐Hyun Kim, Wooyeol Baek, Jeong‐Kee Yoon, et al. "Self‐Enclosable External Support: Dilation‐Responsive Microshape Programing Prevents Vascular Graft Stenosis (Small 18/2021)." Small 17, no. 18 (May 2021): 2170083. http://dx.doi.org/10.1002/smll.202170083.

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Staecker, Hinrich, Ramin Gabaizadeh, Howard Federoff, and Thomas R. Van De Water. "Brain-derived neurotrophic factor gene therapy prevents spiral ganglion degeneration after hair cell loss." Otolaryngology–Head and Neck Surgery 119, no. 1 (July 1998): 7–13. http://dx.doi.org/10.1016/s0194-5998(98)70194-9.

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Destruction of auditory hair cells results in the secondary degeneration of auditory neurons. This is because of the loss of neurotrophic factor support from the auditory hair cells, namely neurotrophin 3, which is normally produced by the inner hair cells. Both in vitro and in vivo studies have shown that delivery of either neurotrophin 3 or brain-derived neurotrophic factor to these neurons can replace the trophic support supplied by the hair cells and prevent their degeneration. To prevent the degeneration of auditory neurons that occurs after neomycin destruction of the auditory hair cells we used a replication defective herpes simplex-1 vector (HSVbdnflac) to transfect the gene for brain-derived neurotrophic factor into the damaged spiral ganglion. Four weeks after the HSVbdnflac therapy we were able to detect stable functional production of brain-derived neurotrophic factor that supported the survival of auditory neurons and prevented the loss of these neurons because of trophic factor deprivation-induced apoptosis. (Otolaryngol Head Neck Surg 1998;119:7–13.)

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Weslow-Schmidt, Janet, Fang Ye, Stephanie S. Cush, Kathleen A. Stuller, Marcia A. Blackman, and Emilio Flaño. "Dendritic Cells Loaded with Tumor B Cells Elicit Broad Immunity against Murine Gammaherpesvirus 68 but Fail To Prevent Long-Term Latency." Journal of Virology 84, no. 17 (June 30, 2010): 8975–79. http://dx.doi.org/10.1128/jvi.00571-10.

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ABSTRACT It is still unknown whether a noninfectious gammaherpesvirus vaccine is able to prevent or reduce virus persistence. This led us to use dendritic cells loaded with tumor B cells as a vaccine approach for the murine gammaherpesvirus 68 (γHV68) model of infection. Dendritic cells loaded with UV-irradiated latently infected tumor B cells induce broad, strong, and long-lasting immunity against γHV68. Dendritic cell vaccination prevents the enlargement of lymph nodes and severely limits acute infection and early latency but does not prevent γHV68 from establishing long-term latency. Our findings support the concept that attenuated viruses may be the best vaccine option for preventing gammaherpesvirus persistence.

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De Moor, Aldo, and Hans Weigand. "Business Negotiation Support: Theory and Practice." International Negotiation 9, no. 1 (2004): 31–57. http://dx.doi.org/10.1163/1571806041262106.

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AbstractBusiness negotiation support systems (NSS) are slowly entering the market, although they lack a clear theoretical basis as of yet. Negotiation is a complicated process with many aspects that have only partially been described with the formal rigidity needed to build support systems. Most theories about negotiation are descriptive and not prescriptive, which, among other things, prevents their use as a basis for negotiation support systems. Complicating matters is that a negotiation process consists of several distinct stages, each with its own characteristics. Furthermore, there are many types of negotiations, depending on the domain. This suggests that we should not strive for one general negotiation support system, but for a set of domain-specific tools. To ground the development and application of these tools in different scenarios, we propose an integrated theoretical framework. After presenting an overview of existing negotiation support approaches, we construct a business negotiation support metamodel for NSS analysis. The metamodel is illustrated by analyzing the MeMo project, which concerns contract negotiations in small and medium enterprises in the European construction industry. The MeMo system is one of the first business NSS with an explicit international orientation.

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Giacomini, Matteo, Gaetano Iapichino, Marco Cigada, Aldo Minuto, Rebecca Facchini, Andrea Noto, and Elena Assi. "Short-term Noninvasive Pressure Support Ventilation Prevents ICU Admittance in Patients With Acute Cardiogenic Pulmonary Edemaa." Chest 123, no. 6 (June 2003): 2057–61. http://dx.doi.org/10.1378/chest.123.6.2057.

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Forbes, Andrew D. "Mechanical Circulatory Support During Repair of Thoracic Aortic Injuries Improves Morbidity and Prevents Spinal Cord Injury." Archives of Surgery 129, no. 5 (May 1, 1994): 494. http://dx.doi.org/10.1001/archsurg.1994.01420290040006.

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Aoyama, A., H. Kinoshita, T. Yoneda, Y. Goda, H. Oda, H. Kayawake, S. Ueda, et al. "Tapering, Not Discontinuation, of Epoprostenol Prevents PGD Requiring ECMO Support in Recipients with Severe Pulmonary Hypertension." Journal of Heart and Lung Transplantation 36, no. 4 (April 2017): S416—S417. http://dx.doi.org/10.1016/j.healun.2017.01.1192.

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Prasad, Joni M., Oleg V. Gorkun, Harini Raghu, Sherry Thornton, Eric S. Mullins, Joseph S. Palumbo, Ya-Ping Ko, et al. "Mice expressing a mutant form of fibrinogen that cannot support fibrin formation exhibit compromised antimicrobial host defense." Blood 126, no. 17 (October 22, 2015): 2047–58. http://dx.doi.org/10.1182/blood-2015-04-639849.

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Key PointsMutation of the fibrinogen Aα chain in mice to selectively eliminate thrombin cleavage prevents fibrin polymer formation in vivo. Fibrin polymer formation drives antimicrobial function and supports host survival following S aureus peritoneal infection.

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Song, Zhilin, Dayane A. Gomes, Wanida Stevens, and Celia D. Sladek. "Multiple α1-adrenergic receptor subtypes support synergistic stimulation of vasopressin and oxytocin release by ATP and phenylephrine." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 6 (December 2010): R1529—R1537. http://dx.doi.org/10.1152/ajpregu.00532.2010.

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Simultaneous exposure of explants of the hypothalamo-neurohypophyseal system (HNS) to ATP and the α1-adrenergic receptor (α1-R) agonist, phenylephrine (ATP+PE) induces a synergistic stimulation of vasopressin and oxytocin (VP/OT) release that is sustained for hours ( 23 ). The current studies confirm that the synergism is dependent upon activation of α1-R by demonstrating that an α1-R antagonist prevents the response. The role of the α1A, B, and D-adrenergic receptor subtypes in the synergistic effect of ATP+PE on intracellular calcium ([Ca2+]i) in supraoptic nucleus (SON) neurons and VP/OT release from neural lobe was evaluated. The increase in [Ca2+]i induced by PE in SON predominantly reflects release from intracellular stores and is mediated by activation of the α1A adrenergic receptor subtype. The α1A subtype is also required for the sustained elevation in [Ca2+]i induced by ATP+PE. In contrast, although synergistic stimulation of VP/OT release was eliminated by removal of PE and was blunted by benoxathian, an α1-R antagonist that is not subtype selective, no single α1-R subtype selective antagonist prevented sustained stimulation of VP/OT release by ATP+PE. Thus, sustained activation of α1-R is essential for the synergistic VP and OT response to ATP+PE, but multiple α1-R subtypes can support the response. Redundancy amongst the α1-R subunits in supporting this response is consistent with the predicted importance of the response for sustaining the elevated VP release required to prevent cardiovascular collapse during hemorrhage and sepsis.

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Bulushev, Dmitri A., Andrey L. Chuvilin, Vladimir I. Sobolev, Svetlana G. Stolyarova, Yury V. Shubin, Igor P. Asanov, Arcady V. Ishchenko, et al. "Copper on carbon materials: stabilization by nitrogen doping." Journal of Materials Chemistry A 5, no. 21 (2017): 10574–83. http://dx.doi.org/10.1039/c7ta02282d.

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Shapiro, Kimron, Jon Driver, Robert Ward, and Robyn E. Sorensen. "Priming from the Attentional Blink: A Failure to Extract Visual Tokens but Not Visual Types." Psychological Science 8, no. 2 (March 1997): 95–100. http://dx.doi.org/10.1111/j.1467-9280.1997.tb00689.x.

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When people must detect several targets in a very rapid stream of successive visual events at the same location, detection of an initial target induces misses for subsequent targets within a brief period. This attentional blink may serve to prevent interruption of ongoing target processing by temporarily suppressing vision for subsequent stimuli. We examined the level at which the internal blink operates, specifically, whether it prevents early visual processing or prevents quite substantial processing from reaching awareness. Our data support the latter view. We observed priming from missed letter targets, benefiting detection of a subsequent target with the same identity but a different case. In a second study, we observed semantic priming from word targets that were missed during the blink. These results demonstrate that attentional gating within the blink operates only after substantial stimulus processing has already taken place. The results are discussed in terms of two forms of visual representation, namely, types and tokens.

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EHIGIATOR, Enoluomen Ben, and Elias ADIKWU. "Ethanolic Extract of Chrysophyllum albidum Stem Bark Prevents Alloxan-Induced Diabetes." Notulae Scientia Biologicae 11, no. 3 (September 30, 2019): 325–31. http://dx.doi.org/10.15835/nsb11310468.

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Chrysophyllum albidum (C. albidum) is traditionally used for the treatment of diabetes, but there is a paucity of scientific evidence to support its use. This study investigated the effect of the ethanolic extract of Chrysophyllum albidum stem bark (EECA) on alloxan-induced diabetic rats. Normal and alloxan-induced diabetic rats were randomly divided into groups and treated with 100-200 mg/kg EECA for 7, 14 and 28 days respectively. Metformin (150 mg/kg) was used as the standard control. Blood samples were collected at the end of treatment for glucose test, while serum samples were extracted and assessed for high density lipoprotein (LDLC), triglyceride (TG) low density lipoprotein cholesterol (LDLC) and total cholesterol (TC). Pancreas was excised and evaluated for oxidative stress indexes. Blood glucose, serum TG, LDL-C and TC levels were significantly (p<0.001) increased whereas HDL-C levels were significantly (p<0.001) decreased in diabetic rats when compared to non-diabetic. Also, pancreatic malondialdehyde levels were significantly (p<0.001) increased whereas superoxide dismutase, glutathione, catalase, and glutathione peroxidase levels were significantly (p<0.001) decreased in diabetic rats when compared to non-diabetic control. However, alterations in the aforementioned parameters were reversed significantly in a dose and time-dependent fashion in diabetic rats treated with 100 mg/kg (p<0.05), 200 mg/kg (p<0.01) and 400 mg/kg (p<0.001) of EECA for 7, 14 and 28 days respectively when compared to diabetic control. EECA showed potential as remedy for diabetes which supports its use in folklore for the treatment of diabetes.

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Pakrieva, Ekaterina, Ekaterina Kolobova, Dmitrii German, Marta Stucchi, Alberto Villa, Laura Prati, Sónia A. C. Carabineiro, Nina Bogdanchikova, Vicente Cortés Corberán, and Alexey Pestryakov. "Glycerol Oxidation over Supported Gold Catalysts: The Combined Effect of Au Particle Size and Basicity of Support." Processes 8, no. 9 (August 20, 2020): 1016. http://dx.doi.org/10.3390/pr8091016.

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Gold nanoparticles supported on various oxides (CeO2, CeO2/TiO2, MgO, MgO/TiO2, La2O3, La2O3/TiO2) (with 4 wt.% Au loading) were investigated in the liquid (aqueous) phase oxidation of glycerol by molecular oxygen under mild conditions, in the presence of alkaline earth (CaO, SrO and MgO) or alkaline (NaOH) bases. Full conversion and selectivity between 38 and 68% to sodium glycerate were observed on different Au supported catalysts (Au/MgO/TiO2, Au/La2O3/TiO2, Au/CeO2 and Au/CeO2/TiO2). The combined effect of Au particle size and basicity of the support was suggested as the determining factor of the activity. Agglomeration of gold nanoparticles, found after the reaction, led to the deactivation of the catalysts, which prevents the further oxidation of sodium glycerate into sodium tartronate. Promising results were obtained with the use of alkaline earth bases (CaO, SrO, MgO), leading to the formation of free carboxylic acids instead of salts, which are formed in the presence of the more usual base, NaOH.

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Xi, Jinkun, Wei Tian, Lei Zhang, Yulan Jin, and Zhelong Xu. "Morphine prevents the mitochondrial permeability transition pore opening through NO/cGMP/PKG/Zn2+/GSK-3β signal pathway in cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H601—H607. http://dx.doi.org/10.1152/ajpheart.00453.2009.

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The aim of this study was to test whether morphine prevents the mitochondrial permeability transition pore (mPTP) opening through Zn2+ and glycogen synthase kinase 3β (GSK-3β). Fluorescence dyes including Newport Green Dichlorofluorescein (DCF), 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM), and tetramethylrhodamine ethyl ester (TMRE) were used to image free Zn2+, nitric oxide (NO), and mitochondrial membrane potential (ΔΨm), respectively. Fluorescence images were obtained with confocal microscopy. Cardiomyocytes treated with morphine for 10 min showed a significant increase in Newport Green DCF fluorescence intensity, an effect that was reversed by the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME), indicating that morphine mobilizes Zn2+ via NO. Morphine rapidly produced NO. ODQ and NS2028, the inhibitors of guanylyl cyclase, prevented Zn2+ release by morphine, implying that cGMP is involved in the action of morphine. The effect of morphine on Zn2+ release was also abolished by KT5823, a specific inhibitor of protein kinase G (PKG). Morphine prevented oxidant-induced loss of ΔΨm, indicating that morphine can modulate the mPTP opening. The effect of morphine on the mPTP was reversed by KT5823 and the Zn2+ chelator N, N, N′, N′-tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN). The action of morphine on the mPTP was lost in cells transfected with the constitutively active GSK-3β mutant, suggesting that morphine may prevent the mPTP opening by inactivating GSK-3β. In support, morphine significantly enhanced phosphorylation of GSK-3β at Ser9, and this was blocked by TPEN. GSK-3β small interfering RNA prevented the pore opening in the control cardiomyocytes but failed to enhance the effect of morphine on the mPTP opening. In conclusion, morphine mobilizes intracellular Zn2+ through the NO/cGMP/PKG signaling pathway and prevents the mPTP opening by inactivating GSK-3β through Zn2+.

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Kottmann, Robert Matthew, Emma Trawick, Jennifer L. Judge, Lindsay A. Wahl, Amali P. Epa, Kristina M. Owens, Thomas H. Thatcher, Richard P. Phipps, and Patricia J. Sime. "Pharmacologic inhibition of lactate production prevents myofibroblast differentiation." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 11 (December 1, 2015): L1305—L1312. http://dx.doi.org/10.1152/ajplung.00058.2015.

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Myofibroblasts are one of the primary cell types responsible for the accumulation of extracellular matrix in fibrosing diseases, and targeting myofibroblast differentiation is an important therapeutic strategy for the treatment of pulmonary fibrosis. Transforming growth factor-β (TGF-β) has been shown to be an important inducer of myofibroblast differentiation. We previously demonstrated that lactate dehydrogenase and its metabolic product lactic acid are important mediators of myofibroblast differentiation, via acid-induced activation of latent TGF-β. Here we explore whether pharmacologic inhibition of LDH activity can prevent TGF-β-induced myofibroblast differentiation. Primary human lung fibroblasts from healthy patients and those with pulmonary fibrosis were treated with TGF-β and or gossypol, an LDH inhibitor. Protein and RNA were analyzed for markers of myofibroblast differentiation and extracellular matrix generation. Gossypol inhibited TGF-β-induced expression of the myofibroblast marker α-smooth muscle actin (α-SMA) in a dose-dependent manner in both healthy and fibrotic human lung fibroblasts. Gossypol also inhibited expression of collagen 1, collagen 3, and fibronectin. Gossypol inhibited LDH activity, the generation of extracellular lactic acid, and the rate of extracellular acidification in a dose-dependent manner. Furthermore, gossypol inhibited TGF-β bioactivity in a dose-dependent manner. Concurrent treatment with an LDH siRNA increased the ability of gossypol to inhibit TGF-β-induced myofibroblast differentiation. Gossypol inhibits TGF-β-induced myofibroblast differentiation through inhibition of LDH, inhibition of extracellular accumulation of lactic acid, and inhibition of TGF-β bioactivity. These data support the hypothesis that pharmacologic inhibition of LDH may play an important role in the treatment of pulmonary fibrosis.

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Lorca, Ramón A., Lorena Varela-Nallar, Nibaldo C. Inestrosa, and J. Pablo Huidobro-Toro. "The Cellular Prion Protein Prevents Copper-Induced Inhibition of P2X4Receptors." International Journal of Alzheimer's Disease 2011 (2011): 1–6. http://dx.doi.org/10.4061/2011/706576.

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Although the physiological function of the cellular prion protein (PrPC) remains unknown, several evidences support the notion of its role in copper homeostasis. PrPCbinds Cu2+through a domain composed by four to five repeats of eight amino acids. Previously, we have shown that the perfusion of this domain prevents and reverses the inhibition by Cu2+of the adenosine triphosphate (ATP)-evoked currents in the P2X4receptor subtype, highlighting a modulatory role for PrPCin synaptic transmission through regulation of Cu2+levels. Here, we study the effect of full-length PrPCin Cu2+inhibition of P2X4receptor when both are coexpressed. PrPCexpression does not significantly change the ATP concentration-response curve in oocytes expressing P2X4receptors. However, the presence of PrPCreduces the inhibition by Cu2+of the ATP-elicited currents in these oocytes, confirming our previous observations with the Cu2+binding domain. Thus, our observations suggest a role for PrPCin modulating synaptic activity through binding of extracellular Cu2+.

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Haanstra, Jurgen R., Arjen van Tuijl, Peter Kessler, Willem Reijnders, Paul A. M. Michels, Hans V. Westerhoff, Marilyn Parsons, and Barbara M. Bakker. "Compartmentation prevents a lethal turbo-explosion of glycolysis in trypanosomes." Proceedings of the National Academy of Sciences 105, no. 46 (November 13, 2008): 17718–23. http://dx.doi.org/10.1073/pnas.0806664105.

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ATP generation by both glycolysis and glycerol catabolism is autocatalytic, because the first kinases of these pathways are fuelled by ATP produced downstream. Previous modeling studies predicted that either feedback inhibition or compartmentation of glycolysis can protect cells from accumulation of intermediates. The deadly parasite Trypanosoma brucei lacks feedback regulation of early steps in glycolysis yet sequesters the relevant enzymes within organelles called glycosomes, leading to the proposal that compartmentation prevents toxic accumulation of intermediates. Here, we show that glucose 6-phosphate indeed accumulates upon glucose addition to PEX14 deficient trypanosomes, which are impaired in glycosomal protein import. With glycerol catabolism, both in silico and in vivo, loss of glycosomal compartmentation led to dramatic increases of glycerol 3-phosphate upon addition of glycerol. As predicted by the model, depletion of glycerol kinase rescued PEX14-deficient cells of glycerol toxicity. This provides the first experimental support for our hypothesis that pathway compartmentation is an alternative to allosteric regulation.

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Giridharan, Guruprasad A., Carlo R. Bartoli, Paul A. Spence, Robert D. Dowling, and Steven C. Koenig. "Counterpulsation With Symphony Prevents Retrograde Carotid, Aortic, and Coronary Flows Observed With Intra-Aortic Balloon Pump Support." Artificial Organs 36, no. 7 (May 16, 2012): 600–606. http://dx.doi.org/10.1111/j.1525-1594.2012.01456.x.

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Isemann, Simon D., Eva Walther, Sara Solfrank, and Felix Wilbertz. "Peacefully changing the world: Political system support facilitates peaceful but prevents violent protest orientation among school students." Peace and Conflict: Journal of Peace Psychology 25, no. 4 (November 2019): 364–66. http://dx.doi.org/10.1037/pac0000388.

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Ehrenkranz, N. Joel. "Bland Soap Handwash or Hand Antisepsis? The Pressing Need for Clarity." Infection Control & Hospital Epidemiology 13, no. 5 (May 1992): 299–304. http://dx.doi.org/10.1086/646531.

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A pervasive misconception in infection control circles is that simple bland soap handwash reliably prevents hand transmission of transiently acquired bacteria, disregarding the level of hand contamination. Often cited to support this widespread misapprehension is a bigger misconception-the efficacy of bland soap handwash is rooted in the epidemiological research of Ignaz Semmelweis. As emphasized by Walter and Beck, Semmelweis did no such thing. Indeed, it was the observation by Semmelweis of failure of bland soap handwash to prevent healthcare workers from spreading puerperal sepsis that led to his investigations of chlorine hand antisepsis for control of cross-infection. These studies ultimately resulted in his demonstrating that effective hand antisepsis (and not bland soap handwash) could prevent transmission of the agents of postpartum endometritis, sepsis, and death.

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Heman-Ackah, Selena E., Tina C. Huang, and Steven K. Juhn. "R442 – Antioxidant Therapy Prevents Presbycusis In C57BL6 mice." Otolaryngology–Head and Neck Surgery 139, no. 2_suppl (August 2008): P192. http://dx.doi.org/10.1016/j.otohns.2008.05.598.

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Problem Presbycusis, or age-related hearing loss, is characterized by gradual, progressive sensorineural hearing loss which accompanies aging with associated decreased speech recognition in noisy environments, slowed central processing of acoustic stimuli and impaired sound localization. In addition to impairing one's ability to communicate effectively, presbycusis jeopardizes one's autonomy, presents a safety concern and has been correlated with an increased incidence of clinical depression and social withdrawal. By 2025, it is estimated that approximately 25 million Americans will be affected, thus this presents a major public health concern. The purpose of this study is to evaluate the potential of antioxidant therapy, including two novel antioxidants, in the prevention of presbycusis. Methods C57BL6 mice were assigned to treatment or control groups. Treatment groups of mice were fed with a combination of two novel antioxidants, L-cysteine-glutathione mixed disulfide and ribose cysteine, as well as vitamin B12, folic acid, and ascorbic acid. Auditory brainstem response thresholds were recorded at baseline and on a monthly basis following initiation of treatment. Results Threshold shifts were observed according to the established pattern of age related loss associated with C57BL6 mice. Threshold shifts were decreased in the treatment group. Statistically significant differences (p<0.001) in threshold shifts were observed between the treatment and control groups for click stimulus and pure tones at 4, 8, 12, 16 and 32 kHz. The treatment group was found to have a smaller degree of shift in association with aging. Conclusion Combination antioxidant therapy effectively decreased threshold shifts on auditory brainstem responses within the established animal model for presbycusis. Significance Combination antioxidant therapy may prove a safe and cost-effective method of preventing presbycusis in our growing elderly population. Support American Academy of Otolaryngology – Head and Neck Surgery Foundation Resident Research Grant.

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Rosenberg, Mark E., Richard Girton, David Finkel, David Chmielewski, Arthur Barrie, David P. Witte, Guang Zhu, John J. Bissler, Judith A. K. Harmony, and Bruce J. Aronow. "Apolipoprotein J/Clusterin Prevents a Progressive Glomerulopathy of Aging." Molecular and Cellular Biology 22, no. 6 (March 15, 2002): 1893–902. http://dx.doi.org/10.1128/mcb.22.6.1893-1902.2002.

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ABSTRACT Apoliprotein J (apoJ)/clusterin has attracted considerable interest based on its inducibility in multiple injury processes and accumulation at sites of remodeling, regression, and degeneration. We therefore sought to investigate apoJ/clusterin's role in kidney aging, as this may reveal the accumulated effects of diminished protection. Aging mice deficient in apoJ/clusterin developed a progressive glomerulopathy characterized by the deposition of immune complexes in the mesangium. Up to 75% of glomeruli in apoJ/clusterin-deficient mice exhibited moderate to severe mesangial lesions by 21 months of age. Wild-type and hemizygous mice exhibited little or no glomerular pathology. In the apoJ/clusterin-deficient mice, immune complexes of immunoglobulin G (IgG), IgM, IgA, and in some cases C1q, C3, and C9 were detectable as early as 4 weeks of age. Electron microscopy revealed the accumulation of electron-dense material in the mesangial matrix and age-dependent formation of intramesangial tubulo-fibrillary structures. Even the most extensively damaged glomeruli showed no evidence of inflammation or necrosis. In young apoJ/clusterin-deficient animals, the development of immune complex lesions was accelerated by unilateral nephrectomy-induced hyperfiltration. Injected immune complexes localized to the mesangium of apoJ/clusterin-deficient but not wild-type mice. These results establish a protective role of apoJ/clusterin against chronic glomerular kidney disease and support the hypothesis that apoJ/clusterin modifies immune complex metabolism and disposal.

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Liu, Yan, Soren M. Johnson, Yuri Fedoriw, Arlin B. Rogers, Hong Yuan, Janakiraman Krishnamurthy, and Norman E. Sharpless. "Expression of p16INK4a prevents cancer and promotes aging in lymphocytes." Blood 117, no. 12 (March 24, 2011): 3257–67. http://dx.doi.org/10.1182/blood-2010-09-304402.

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Abstract Previous authors have suggested that tumor suppressor expression promotes aging while preventing cancer, but direct experimental support for this cancer-aging hypothesis has been elusive. Here, by using somatic, tissue-specific inactivation of the p16INK4a tumor suppressor in murine T- or B-lymphoid progenitors, we report that ablation of p16INK4a can either rescue aging or promote cancer in a lineage-specific manner. Deletion of p16INK4a in the T lineage ameliorated several aging phenotypes, including thymic involution, decreased production of naive T cells, reduction in homeostatic T-cell proliferation, and attenuation of antigen-specific immune responses. Increased T-cell neoplasia was not observed with somatic p16INK4a inactivation in T cells. In contrast, B lineage–specific ablation of p16INK4a was associated with a markedly increased incidence of systemic, high-grade B-cell neoplasms, which limited studies of the effects of somatic p16INK4a ablation on B-cell aging. Together, these data show that expression of p16INK4a can promote aging and prevent cancer in related lymphoid progeny of a common stem cell.

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Radke, Oliver C., Thomas Schneider, Axel R. Heller, and Thea Koch. "Spontaneous Breathing during General Anesthesia Prevents the Ventral Redistribution of Ventilation as Detected by Electrical Impedance Tomography." Anesthesiology 116, no. 6 (June 1, 2012): 1227–34. http://dx.doi.org/10.1097/aln.0b013e318256ee08.

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Background Positive-pressure ventilation causes a ventral redistribution of ventilation. Spontaneous breathing during general anesthesia with a laryngeal mask airway could prevent this redistribution of ventilation. We hypothesize that, compared with pressure-controlled ventilation, spontaneous breathing and pressure support ventilation reduce the extent of the redistribution of ventilation as detected by electrical impedance tomography. Methods The study was a randomized, three-armed, observational, clinical trial without blinding. With approval from the local ethics committee, we enrolled 30 nonobese patients without severe cardiac or pulmonary comorbidities who were scheduled for elective orthopedic surgery. All of the procedures were performed under general anesthesia with a laryngeal mask airway and a standardized anesthetic regimen. The center of ventilation (primary outcome) was calculated before the induction of anesthesia (AWAKE), after the placement of the laryngeal mask airway (BEGIN), before the end of anesthesia (END), and after arrival in the postanesthesia care unit (PACU). Results The center of ventilation during anesthesia (BEGIN) was higher than baseline (AWAKE) in both the pressure-controlled and pressure support ventilation groups (pressure control: 55.0 vs. 48.3, pressure support: 54.7 vs. 48.8, respectively; multivariate analysis of covariance, P < 0.01), whereas the values in the spontaneous breathing group remained at baseline levels (47.9 vs. 48.5). In the postanesthesia care unit, the center of ventilation had returned to the baseline values in all groups. No adverse events were recorded. Conclusions Both pressure-controlled ventilation and pressure support ventilation induce a redistribution of ventilation toward the ventral region, as detected by electrical impedance tomography. Spontaneous breathing prevents this redistribution.

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Garicano, Luis, and Tano Santos. "Referrals." American Economic Review 94, no. 3 (May 1, 2004): 499–525. http://dx.doi.org/10.1257/0002828041464506.

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This paper studies the matching of opportunities with talent when costly diagnosis confers an informational advantage to the agent undertaking it. When this agent is underqualified, adverse selection prevents efficient referrals through fixed-price contracts. Spot-market contracts that rely on income sharing can match opportunities with talent but induce a team-production problem which, if severe enough, can prevent the referral of valuable opportunities. Partnership contracts, in which agents agree in advance to the allocation of opportunities and of the revenues they generate, support referrals where the market cannot, but often at the expense of distortions on those opportunities that are not referred.

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Nishizawa, Kenya, Paul E. Wolkowicz, Tadashi Yamagishi, Ling-Ling Guo, and Martin M. Pike. "Fasudil prevents KATP channel-induced improvement in postischemic functional recovery." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H3011—H3015. http://dx.doi.org/10.1152/ajpheart.00611.2004.

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Whereas activation of ATP-dependent potassium (KATP) channels greatly improves postischemic myocardial recovery, the final effector mechanism for KATP channel-induced cardioprotection remains elusive. RhoA is a GTPase that regulates a variety of cellular processes known to be involved with KATP channel cardioprotection. Our goal was to determine whether the activity of a key rhoA effector, rho kinase (ROCK), is required for KATP channel-induced cardioprotection. Four groups of perfused rat hearts were subjected to 36 min of zero-flow ischemia and 44 min of reperfusion with continuous measurements of mechanical function and 31P NMR high-energy phosphate data: 1) untreated, 2) pinacidil (10 μM) to activate KATP channels, 3) fasudil (15 μM) to inhibit ROCK, and 4) both fasudil and pinacidil. Pinacidil significantly improved postischemic mechanical recovery [39 ± 16 vs. 108 ± 4 mmHg left ventricular diastolic pressure (LVDP), untreated and pinacidil, respectively]. Fasudil did not affect reperfusion LVDP (41 ± 13 mmHg) but completely blocked the marked improvement in mechanical recovery that occurred with pinacidil treatment (54 ± 15 mmHg). Substantial attenuation of the postischemic energetic recovery was also observed. These data support the hypothesis that ROCK activity plays a role in KATP channel-induced cardioprotection.

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Phillips, P. G., H. Lum, A. B. Malik, and M. F. Tsan. "Phallacidin prevents thrombin-induced increases in endothelial permeability to albumin." American Journal of Physiology-Cell Physiology 257, no. 3 (September 1, 1989): C562—C567. http://dx.doi.org/10.1152/ajpcell.1989.257.3.c562.

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Calf pulmonary artery endothelial monolayers cultured on polycarbonate filters were utilized to study 125I-labeled albumin permeability and actin filament distribution in response to thrombin challenge. Thirty-minute exposure to alpha-thrombin (10(-7) M) significantly increased albumin clearance rates. These changes were associated with marked alterations in actin filament distribution, resulting in loss of peripheral actin bands and an increase in the number of cytoplasmic stress fibers. Because the actin peripheral filaments are thought to play an important role in junctional stability, we postulated that stabilization of actin filaments should protect against thrombin-induced barrier disruptions. Pretreatment of cells with 0.3 microM 7-nitrobenz-2-oxa-1,3-diazole (NBD)-phallacidin, a specific actin-stabilizing agent, prevented the changes in actin filament distribution and markedly attenuated the increase in albumin permeability. Because of the potential toxicity of phallatoxins, we evaluated the effects of pretreatment on cell viability and growth parameters. There were no differences in viability, seeding efficiency, or doubling times in cells treated with 0.3 microM NBD-phallacidin in comparison to controls. Our data support the hypothesis that actin filaments, particularly peripheral bands, contribute significantly to the maintenance of barrier function in cultured endothelial cells.

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Tiganos, E., and M. B. Herrington. "Kasugamycin inhibition of nonsense suppression by thymine-requiring strains of Escherichia coli K12." Canadian Journal of Microbiology 39, no. 4 (April 1, 1993): 448–50. http://dx.doi.org/10.1139/m93-065.

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Thymine-requiring strains of Escherichia coli suppress nonsense and frame-shift mutations. This appears to occur during translation, suggesting that the lack of activity of an enzyme thymidylate synthase, required for the synthesis of a DNA precursor, alters the fidelity of translation. The aminoglycoside antibiotic kasugamycin, which enhances translational accuracy in vitro, prevents thymine-requiring cells from suppressing. The inhibition of suppression by kasugamycin is not prevented by the introduction of two different kasugamycin-resistance mutations, although the dose required for inhibition increases. These observations support the conclusion that suppression occurs during translation.Key words: suppression, kasugamycin, translation, thymine-requiring.

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Watts, Bruns A., Esther Tamayo, Edward R. Sherwood, and David W. Good. "Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through induction of Tollip and negative regulation of IRAK-1." American Journal of Physiology-Renal Physiology 317, no. 3 (September 1, 2019): F705—F719. http://dx.doi.org/10.1152/ajprenal.00170.2019.

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LPS inhibits [Formula: see text] absorption in the medullary thick ascending limb (MTAL) through a Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-extracellular signal-regulated kinase (ERK) pathway that is upregulated by sepsis. Pretreatment with the nontoxic immunomodulator monophosphoryl lipid A (MPLA) prevents inhibition by LPS through activation of a TLR4-TIR-domain-containing adaptor-inducing interferon-β (TRIF)-phosphatidylinositol 3-kinase (PI3K) pathway that prevents LPS-induced ERK activation. Here, we identified the molecular mechanisms that underlie the protective inhibitory interaction between the MPLA-PI3K and LPS-ERK pathways. Treatment of mouse MTALs with LPS in vitro increased phosphorylation of IL-1 receptor-associated kinase (IRAK)-1, a critical mediator of LPS signaling downstream of TLR4-MyD88. Activation of ERK by LPS was eliminated by a selective IRAK-1 inhibitor, establishing IRAK-1 as the upstream mediator of ERK activation. Pretreatment of MTALs with MPLA in vitro prevented LPS-induced IRAK-1 activation; this effect was dependent on PI3K. Treatment of MTALs with MPLA increased expression of Toll-interacting protein (Tollip), an inducible protein that negatively regulates LPS signaling by inhibiting IRAK-1. The MPLA-induced increase in Tollip protein level was prevented by PI3K inhibitors. In coimmunoprecipitation experiments, MPLA increased the amount of Tollip stably bound to IRAK-1, an interaction that inhibits IRAK-1 activation. These results support a mechanism whereby MPLA increases Tollip expression in the MTAL through a PI3K-dependent pathway. Tollip, in turn, inhibits LPS-induced TLR4 signaling by suppressing activation of IRAK-1, thereby preventing activation of ERK that inhibits [Formula: see text] absorption. These studies show that MPLA induces reprogramming of MTAL cells that protects against LPS stimulation and identify IRAK-1 and Tollip as new therapeutic targets to prevent renal tubule dysfunction in response to infectious and inflammatory stimuli.

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Buster, Dan, Karen McNally, and Francis J. McNally. "Katanin inhibition prevents the redistribution of γ-tubulin at mitosis." Journal of Cell Science 115, no. 5 (March 1, 2002): 1083–92. http://dx.doi.org/10.1242/jcs.115.5.1083.

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Katanin is a microtubule-severing protein that is concentrated at mitotic spindle poles but katanin's function in the mitotic spindle has not been previously reported. Inhibition of katanin with either of two dominant-negative proteins or a subunit-specific antibody prevented the redistribution of γ-tubulin from the centrosome to the spindle in prometaphase CV-1 cells as assayed by immunofluorescence microscopy. Becauseγ-tubulin complexes can bind to pre-existing microtubule minus ends,these results could be explained by a model in which the broad distribution ofγ-tubulin in the mitotic spindle is in part due to cytosolicγ-tubulin ring complexes binding to microtubule minus ends generated by katanin-mediated microtubule severing. Because microtubules depolymerize at their ends, we hypothesized that a greater number of microtubule ends generated by severing in the spindle would result in an increased rate of spindle disassembly when polymerization is blocked with nocodazole. Indeed,katanin inhibition slowed the rate of spindle microtubule disassembly in the presence of nocodazole. However, katanin inhibition did not affect the rate of exchange between polymerized and unpolymerized tubulin as assayed by fluorescence recovery after photobleaching. These results support a model in which katanin activity regulates the number of microtubule ends in the spindle.

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Djaya, Nanny, Jimmy Barus, and Flora. "FERMENTED SOYBEAN CAKE AND ALBUMIN FORMULA AS NUTRITIONAL SUPPORT PREVENTS PROTEIN ENERGY MALNUTRITION AND AKI IN STROKE PATIENTS." Kidney Research and Clinical Practice 31, no. 2 (June 2012): A28. http://dx.doi.org/10.1016/j.krcp.2012.04.373.

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DE CURTIS, A., S. MURZILLI, A. DI CASTELNUOVO, D. ROTILIO, M. B. DONATI, G. DE GAETANO, and L. IACOVIELLO. "Alcohol-free red wine prevents arterial thrombosis in dietary-induced hypercholesterolemic rats: experimental support for the 'French paradox'." Journal of Thrombosis and Haemostasis 3, no. 2 (February 2005): 346–50. http://dx.doi.org/10.1111/j.1538-7836.2005.01126.x.

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Qavi, Abraham, Jeffrey Szymanski, and Ronald Jackups. "17 A Clinical Decision Support Alert Prevents Inappropriate Repeat Laboratory Testing Ordered Within the Same Admission on Inpatients." American Journal of Clinical Pathology 149, suppl_1 (January 2018): S172. http://dx.doi.org/10.1093/ajcp/aqx149.386.

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Chanoit, Guillaume, SungRyul Lee, Jinkun Xi, Min Zhu, Rachel A. McIntosh, Robert A. Mueller, Edward A. Norfleet, and Zhelong Xu. "Exogenous zinc protects cardiac cells from reperfusion injury by targeting mitochondrial permeability transition pore through inactivation of glycogen synthase kinase-3β." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H1227—H1233. http://dx.doi.org/10.1152/ajpheart.00610.2008.

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The purpose of this study was to determine whether exogenous zinc prevents cardiac reperfusion injury by targeting the mitochondrial permeability transition pore (mPTP) via glycogen synthase kinase-3β (GSK-3β). The treatment of cardiac H9c2 cells with ZnCl2 (10 μM) in the presence of zinc ionophore pyrithione for 20 min significantly enhanced GSK-3β phosphorylation at Ser9, indicating that exogenous zinc can inactivate GSK-3β in H9c2 cells. The effect of zinc on GSK-3β activity was blocked by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY-294002 but not by the mammalian target of rapamycin (mTOR) inhibitor rapamycin or the PKC inhibitor chelerythrine, implying that PI3K but not mTOR or PKC accounts for the action of zinc. In support of this interpretation, zinc induced a significant increase in Akt but not mTOR phosphorylation. Further experiments found that zinc also increased mitochondrial GSK-3β phosphorylation. This may indicate an involvement of the mitochondria in the action of zinc. The effect of zinc on mitochondrial GSK-3β phosphorylation was not altered by the mitochondrial ATP-sensitive K+ channel blocker 5-hydroxydecanoic acid. Zinc applied at reperfusion reduced cell death in cells subjected to simulated ischemia/reperfusion, indicating that zinc can prevent reperfusion injury. However, zinc was not able to exert protection in cells transfected with the constitutively active GSK-3β (GSK-3β-S9A-HA) mutant, suggesting that zinc prevents reperfusion injury by inactivating GSK-3β. Cells transfected with the catalytically inactive GSK-3β (GSK-3β-KM-HA) also revealed a significant decrease in cell death, strongly supporting the essential role of GSK-3β inactivation in cardioprotection. Moreover, zinc prevented oxidant-induced mPTP opening through the inhibition of GSK-3β. Taken together, these data suggest that zinc prevents reperfusion injury by modulating the mPTP opening through the inactivation of GSK-3β. The PI3K/Akt signaling pathway is responsible for the inactivation of GSK-3β by zinc.

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Wannapakdee, Wannaruedee, Thittaya Yutthalekha, Pannida Dugkhuntod, Kamonlatth Rodponthukwaji, Anawat Thivasasith, Somkiat Nokbin, Thongthai Witoon, Sitthiphong Pengpanich, and Chularat Wattanakit. "Dehydrogenation of Propane to Propylene Using Promoter-Free Hierarchical Pt/Silicalite-1 Nanosheets." Catalysts 9, no. 2 (February 13, 2019): 174. http://dx.doi.org/10.3390/catal9020174.

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Propane dehydrogenation (PDH) is the extensive pathway to produce propylene, which is as a very important chemical building block for the chemical industry. Various catalysts have been developed to increase the propylene yield over recent decades; however, an active site of monometallic Pt nanoparticles prevents them from achieving this, due to the interferences of side-reactions. In this context, we describe the use of promoter-free hierarchical Pt/silicalite-1 nanosheets in the PDH application. The Pt dispersion on weakly acidic supports can be improved due to an increase in the metal-support interaction of ultra-small metal nanoparticles and silanol defect sites of hierarchical structures. This behavior leads to highly selective propylene production, with more than 95% of propylene selectivity, due to the complete suppression of the side catalytic cracking. Moreover, the oligomerization as a side reaction is prevented in the presence of hierarchical structures due to the shortening of the diffusion path length.

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van Acker, Gijs J. D., Ashok K. Saluja, Lakshmi Bhagat, Vijay P. Singh, Albert M. Song, and Michael L. Steer. "Cathepsin B inhibition prevents trypsinogen activation and reduces pancreatitis severity." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 3 (September 1, 2002): G794—G800. http://dx.doi.org/10.1152/ajpgi.00363.2001.

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Intrapancreatic activation of trypsinogen is believed to play a critical role in the initiation of acute pancreatitis, but mechanisms responsible for intrapancreatic trypsinogen activation during pancreatitis have not been clearly defined. In previous in vitro studies, we have shown that intra-acinar cell activation of trypsinogen and acinar cell injury in response to supramaximal secretagogue stimulation could be prevented by the cell permeant cathepsin B inhibitor E64d (Saluja A, Donovan EA, Yamanaka K, Yamaguchi Y, Hofbauer B, and Steer ML. Gastroenterology 113: 304–310, 1997). The present studies evaluated the role of intrapancreatic trypsinogen activation, this time under in vivo conditions, in two models of pancreatitis by using another highly soluble cell permeant cathepsin B inhibitor,l-3-trans-(propylcarbamoyl)oxirane-2-carbonyl-l-isoleucyl-l-proline methyl ester (CA-074me). Intravenous administration of CA-074me (10 mg/kg) before induction of either secretagogue-elicited pancreatitis in mice or duct infusion-elicited pancreatitis in rats markedly reduced the extent of intrapancreatic trypsinogen activation and substantially reduced the severity of both pancreatitis models. These observations support the hypothesis that, during the early stages of pancreatitis, trypsinogen activation in the pancreas is mediated by the lysosomal enzyme cathepsin B. Our findings also suggest that pharmacological interventions that inhibit cathepsin B may prove useful in preventing acute pancreatitis or reducing its severity.

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Journal articles on the topic 'Support prevents'

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