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Relevant bibliographies by topics / Ethanol Ethanol Opioid peptides

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Academic literature on the topic 'Ethanol Ethanol Opioid peptides'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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Journal articles on the topic "Ethanol Ethanol Opioid peptides"

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Goldberg, Joel S. "Low Molecular Weight Opioid Peptide Esters Could be Developed as a New Class of Analgesics." Perspectives in Medicinal Chemistry 5 (January 2011): PMC.S6803. http://dx.doi.org/10.4137/pmc.s6803.

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Low molecular weight opioid peptide esters (OPE) could become a class of analgesics with different side effect profiles than current opiates. OPE may have sufficient plasma stability to cross the blood brain barrier (BBB), undergo ester hydrolysis and produce analgesia. OPE of dipeptides, tyr-pro and tyr-gly conjugated to ethanol have a structure similar to the anesthestic agent, etomidate. Based upon the analgesic activity of dipeptide opioids, Lipinski's criteria, and permeability of select GABA esters to cross the BBB, opioid peptides (OP) conjugated to ethanol, cholesterol or 3-glucose are lead recommendations. Preliminary animal data suggests that tyr-pro-ethyl ester crosses the BBB and unexpectedly produces hyperalgesia. Currently, there are no approved OP analgesics available for clinical use. Clinical trials of good manufacturing practice OP administered to patients suffering from chronic pain with indwelling intrathecal pumps could resolve the issue that OP may be superior to opiates and may redirect research.

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Coiro, V., A. Alboni, D. Gramellini, C. Cigarini, L. Bianconi, D. Pignatti, R. Volpi, and P. Chiodera. "Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids." Acta Endocrinologica 126, no. 3 (March 1992): 213–16. http://dx.doi.org/10.1530/acta.0.1260213.

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The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

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Gianoulakis, C. "The effect of ethanol on the biosynthesis and regulation of opioid peptides." Experientia 45, no. 5 (May 1989): 428–35. http://dx.doi.org/10.1007/bf01952024.

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Chang, Guo-Qing, Olga Karatayev, Rashedul Ahsan, Nicole M. Avena, Caroline Lee, Michael J. Lewis, Bartley G. Hoebel, and Sarah F. Leibowitz. "Effect of Ethanol on Hypothalamic Opioid Peptides, Enkephalin, and Dynorphin: Relationship With Circulating Triglycerides." Alcoholism: Clinical and Experimental Research 31, no. 2 (February 2007): 249–59. http://dx.doi.org/10.1111/j.1530-0277.2006.00312.x.

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Przewłocka, Barbara, Wiadysław Lasoń, and Ryszard Przewłocki. "Repeated Ethanol Differently Affects Opioid Peptide Biosynthesis in the Rat Pituitary." Neuroendocrinology 60, no. 3 (1994): 331–36. http://dx.doi.org/10.1159/000126766.

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Palm, Sara, Erika Roman, and Ingrid Nylander. "Differences in basal and ethanol-induced levels of opioid peptides in Wistar rats from five different suppliers." Peptides 36, no. 1 (July 2012): 1–8. http://dx.doi.org/10.1016/j.peptides.2012.04.016.

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Gustafsson, L., Q. Zhou, and I. Nylander. "Ethanol-induced effects on opioid peptides in adult male Wistar rats are dependent on early environmental factors." Neuroscience 146, no. 3 (May 2007): 1137–49. http://dx.doi.org/10.1016/j.neuroscience.2007.02.037.

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Boyadjieva, Nadka, Madhavi Dokur, Juan P. Advis, Gary G. Meadows, and Dipak K. Sarkar. "Chronic Ethanol Inhibits NK Cell Cytolytic Activity: Role of Opioid Peptide β-Endorphin." Journal of Immunology 167, no. 10 (November 15, 2001): 5645–52. http://dx.doi.org/10.4049/jimmunol.167.10.5645.

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Jarjour, Samuel, Li Bai, and Christina Gianoulakis. "Effect of Acute Ethanol Administration on the Release of Opioid Peptides From the Midbrain Including the Ventral Tegmental Area." Alcoholism: Clinical and Experimental Research 33, no. 6 (June 2009): 1033–43. http://dx.doi.org/10.1111/j.1530-0277.2009.00924.x.

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Przewo̵cka, B., W. Lasoń, and R. Przewlocki. "Effect of repeated ethanol administration on opioid peptide systems activity in rat hypothalamus and pituitary." Pharmacological Research 25 (May 1992): 71–72. http://dx.doi.org/10.1016/1043-6618(92)90292-j.

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Dissertations / Theses on the topic "Ethanol Ethanol Opioid peptides"

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Ploj, Karolina. "Involvement of the Opioid System in High Alcohol Consumption : Environmental and Genetic Influences." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5217-5/.

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Gustafsson, Lisa. "Endogenous Opioids and Voluntary Ethanol Drinking : Consequences of Postnatal Environmental Influences in Rats." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7776.

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Jarjour, Samuel J. "Effect of acute ethanol administration on the extracellular concentrations of the opioid peptides [beta]-endorphin, met-enkephalin and dynorphin A₁-₈ at the level of ventral tegmental area in the rat." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101719.

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There is experimental evidence suggesting that ethanol alters the activity of the endogenous opioid peptide systems in a dose and brain region dependent manner. These ethanol-induced alterations in opioid activity may influence the processes of ethanol reward and reinforcement. However, the precise nature of the link between ethanol-opioid interactions influencing reward and reinforcement is not clearly understood. Thus, it was the objective of the present study to investigate the response of the three major opioid peptide systems (endorphins, enkephalins, and dynorphins) to acute ethanol administration, at the level of the ventral tegmental area (VTA), a brain region important for drug, including ethanol, reinforcement. Using the in vivo microdialysis technique coupled with specific solid-phase radioimmunoassays for beta-endorphin, met-enkephalin, and dynorphin A1-8, changes of the extracellular concentration of theses peptides at the level of VTA were determined at distinct time points following the administration of 0.0 (saline), 0.8, 1.6, and 2.4 g ethanol/kg B/Wt. Results demonstrated a biphasic effect of ethanol on beta-endorphin release with 1.6, but not 0.8 or 2.4, g ethanol/kg B.Wt. enhancing beta-endorphin release. None of the ethanol doses used altered the extracellular levels of met-enkephalin, and dynorphin A1-8 peptides. In conclusion, the present findings suggest that at the level of VTA interactions of beta-endorphin with the mu and/or delta opioid receptors on GABA interneurons may contribute to the ethanol induced augmentation in the activity of the mesolimbic dopaminergic system, and influence ethanol reinforcement.

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Rosin, Åsa. "Effects of joint cocaine and ethanol on the brain opioid systems /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-441-4/.

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Park, Jung Jae. "Does Electroacupuncture Affect Ethanol Modulation of Mesolimbic Neurons?" BYU ScholarsArchive, 2010. https://scholarsarchive.byu.edu/etd/2313.

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The purpose of this project was to investigate the mechanism of action of acupuncture on a critical neural substrate involved in alcoholism. Specifically, this study evaluated the effects of stimulation of the acupuncture Shenmen (HT7) point on inhibitory GABA neurons in the ventral tegmental area (VTA), a midbrain structure implicated in drug and alcohol abuse, and ethanol self-administration. In addition, the role of opioid receptors (ORs) in ethanol and acupuncture effects was explored. Using electrophysiological methods in mature rats, we evaluated the effects of HT7 stimulation and opioid antagonists on the VTA GABA neuron firing rate. With behavioral paradigms, we also assessed those effects on ethanol self-administration, using a modification of the sucrose fading procedure. We found that HT7 stimulation produced a biphasic modulation of VTA GABA neuron firing rate characterized by transient enhancement at the onset of stimulation followed by a prolonged inhibition and subsequent recovery in 5 min. HT7 stimulation blocked the typical suppression of VTA GABA neuron firing rate produced by a moderately intoxicating dose of ethanol. The late inhibition produced by HT7 stimulation as well as HT7 reversal of ethanol's effects on GABA neuron firing rate was blocked by the non-selective opioid receptor antagonist, naloxoneIn addition, HT7 acupuncture reduced ethanol self-administration without affecting sucrose consumption. More important, systemic administration of the δ-opioid receptor (DOR) antagonist, naltrindole blocked ethanol suppression of VTA GABA neuron firing rate and significantly reduced ethanol self-administration without affecting sucrose consumption. These findings suggest that DOR-mediated opioid modulation of VTA GABA neurons may be related to the role of acupuncture in modulating mesolimbic DA release and suppressing the reinforcing effects of ethanol. We confirmed that acupuncture stimulation may have a significant impact on the inhibitory neuron activity in the VTA and that acupuncture may serve as an effective adjunct to OR antagonist therapy for alcoholism.

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Knott, Thomas K. "Ethanol Tolerance in the Rat Neurohypophysis: a Dissertation." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/54.

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One of the main components underlying drug addiction is the emergence of tolerance. Although its development is a complex issue, and is believed to have both psychological and physiological connotations, it is clear that some physiological change must occur that would enable an organism to withstand drug concentrations lethal to a naïve system. The purpose of this thesis was to identify and study a physiological mechanism, whose characteristics were altered due to chronic exposure to ethanol. Vasopressin (AVP), whose primary function is to control water balance, release from the neurohypophysis is suppressed by an acute ethanol challenge. Therefore, I hypothesized; 1) that chronic ethanol exposure would reduce the normal suppression of AVP release during an acute ethanol challenge and 2) that the ion channels that are acutely sensitive to ethanol, involved in the control of AVP release, would exhibit a change in their ethanol sensitivity and characteristics. To study the hypothesis, I utilized the neurohypophysis from rats chronically exposed to ethanol and yoked controls to determine whether chronic exposure would modify the acute ethanol sensitivity of the neurohypophysial vasopressin release mechanism. I examined whether the long-term ethanol exposure affected the suppression of vasopressin release from either or both the intact neurohypophysis and the isolated neurohypophysial terminals. In addition, I investigated how chronic exposure affected two types of potassium channels, the ethanol sensitive large conductance Ca+2-activated (BK) channel and the fast inactivating (IA) channel known to be insensitive to physiologically relevant concentrations of ethanol. I was able to establish that chronic ethanol exposure reduced the suppression of vasopressin release by an acute ethanol challenge from both the intact neurohypophysis and the isolated neurohypophysial terminals. In addition, I discovered that oxytocin release was affected similarly. I concluded from this data that chronic exposure to ethanol affected a general mechanism, which controlled hormone release from the neurohypophysis, and that this mechanism could be isolated to the neurohypophysial terminals. I also used electrophysiological techniques to study ion channel characteristics of both the BK and IA potassium channels. I found that in naïve rats, BK channels were potentiated and IA channels insensitive to physiological relevant concentrations of ethanol. But in chronic ethanol-exposed rats the BK channels exhibited a reduced sensitivity to ethanol while IA channels were inhibited. In addition, the current density of the BK channel was significantly reduced. These results show that at least one characteristic of each potassium channel has been modified. This suggests that chronic exposure can not only modify the ethanol sensitivity of ion channels known to be ethanol-sensitive, but also those believed to be relatively insensitive. Therefore, since modifications in these channels have previously been shown to alter the duration and frequency of action potentials, I conclude that these ethanol-induced modifications play a role in the modified hormone release patterns observed in the chronically exposed rats.

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Chow, Yip-chuen. "A study on the ulcerogenic mechanisms of cigarette smoke exposure on ethanol-induced gastric mucosal damage in rats /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19537505.

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周業全 and Yip-chuen Chow. "A study on the ulcerogenic mechanisms of cigarette smoke exposure on ethanol-induced gastric mucosal damage in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31236777.

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Crowley, John J. "Cholesterol and Phospholipid Modulation of BK[subscript Ca] Channel Activity and Ethanol Sensitivity: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/107.

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The large conductance Ca++-activated K+ channel (BKCa) regulates neuronal excitability through the efflux of K+, in response to membrane depolarization and increases in intracellular Ca++. The activity of the BKCa channel is increased by acute exposure to ethanol (EtOH), which is thought to underlie, in part, the influence of the drug on peptide hormone release from neurohypophysial nerve terminals (Dopico et al., 1996, 1998). Moreover, chronic EtOH exposure attenuates acute drug action on hormone release, and reduces the sensitivity of BKCa channels to acute EtOH exposure (Knott et al., 2002). The factors regulating EtOH action on BKCa channels are not well understood. Several lines of evidence suggest, however, that the lipid composition of the plasma membrane may influence channel sensitivity to the drug. The plasma membrane is highly complex in its organization (Welti and Glaser, 1994; Brown and London, 1998). There is a growing body of literature indicating that the local lipid composition of the membrane can influence the function of ion channels, including BKCa (Chang et al., 1995a, b; Moczydlowski et al., 1985; Park et al., 2003; Turnheim et al., 1999). Interestingly, chronic exposure to EtOH in animal models results in alterations in the composition of synaptic plasma membranes, including changes in the amount and distribution of membrane cholesterol (CHS) (Chin et al., 1978; Chin et al., 1979; Wood et al., 1989). The significance of these alterations is unclear. Here, we set out to determine the ability of membrane lipids to modulate BKCa channel activity and EtOH sensitivity. To address this, we implement the planar lipid bilayer technique, allowing control of both the protein and lipid components of the membrane. Native BKCa channels retain EtOH sensitivity in this reductionist preparation (Chu et al., 1998), and we extend the study here to examine cloned human brain (hslo) BKCachannels. We show here that hslo channels maintain their characteristic large conductance, voltage and Ca++-dependent gating, and sensitivity to 50 mM EtOH in bilayers cast from a 3:1 mixture of 1-pamiltoyl-2-oleoyl-phosphatidylethanolamine (POPE) and 1-pamiltoyl-2-oleoyl-phosphatidylserine (POPS). The addition of CHS to the bilayer decreases both the basal activity and EtOH sensitivity of the channels, in a concentration-dependent manner. This lends support to the notion that alterations in plasma membrane CHS levels following chronic EtOH exposure may reflect adaptations to the acute actions of the drug on ion channels. Furthermore, the EtOH sensitivity and CHS modulation of these reconstituted hslo channels are greatly reduced in the absence of negatively charged POPS in the bilayer (pure POPE). Based on these findings, we look to gain mechanistic insight into the lipid headgroup and acyl chain properties that may regulate BKCa channel modulation by EtOH and CHS. When POPS is replaced with the uncharged lipid 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC), the hslo response to EtOH and CHS is restored, suggesting that the loss of negative surface charge or PS headgroup structure itself cannot explain the lack of channel modulation by these agents in POPE bilayers. Moreover, increases in the proportion of unsaturated acyl chains in the bilayer cannot significantly influence the hslo response to EtOH. The loss of EtOH sensitivity in pure POPE and CHS-containing bilayers may, therefore, reflect the propensity of POPE and CHS to form nonlamellar (nonbilayer) structures. Regarding the basal activity of the channel, we demonstrate that decreases in negative surface charge, increases in the proportion of unsaturated acyl chains, and increases in the complexity of head group interactions can all influence the steady-state activity of reconstituted hslochannels, relative to control POPE/POPS (3:1) bilayers. Overall, these data further suggest the ability of the local lipid environment to regulate the basal function and EtOH sensitivity of an ion channel protein. Parts of this dissertation have appeared in separate publications: Treistman, S.N., O'Connell, R.J., and Crowley, J.J. (2002). Artificial Bilayer Techniques in Ion Channel Study. In Methods in Alcohol-Related Neuroscience Research, D. Lovinger and Y. Liu, eds. (Boca Raton, Florida: CRC Press) Crowley, J.J., Treistman, S.N., and Dopico, A.M. (2003). Cholesterol antagonizes ethanol potentiation of human BKCA channels in binary phospholipid bilayers. Mol. Pharma. 64(2):364-372.

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Almeida, Glauco Garrido [UNESP]. "Estudo da dinâmica de solvatação de peptídeos por QM/MM." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/136315.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Trabalhos experimentais e teóricos desenvolvidos nos últimos anos evidenciaram a capacidade de alcoóis e polialcoóis em mudar características energéticas em proteínas. No entanto, o mecanismo responsável por esse efeito não está totalmente elucidado. Tomando como exemplo o dipeptídeo de alanina, foram realizadas simulações QM/MM em água, etanol e mistura 60-40 % em volume de água-etanol. A molécula de dipeptídeo foi descrita em nível de cálculo quântico MP2/aug-cc-pVDZ. Em solução, apenas confórmeros αR e PPII foram encontrados na população de equilíbrio. A diferença de energia livre em solução αR  PPII é determinada pelo balanço entre energia interna do soluto e energia de interação. Para o dipeptídeo de alanina, qualquer fator que aumente a energia de interação soluto-solvente favorece o aumento da população de αR. Por outro lado fatores que diminuam esse valor, como a adição de etanol, aumentam a população de PPII. Os resultados indicam solvatação preferencial para o sistema, evidenciado pela formação majoritária da primeira camada de solvatação por moléculas de água (na mistura), embora seja possível encontrar moléculas de etanol em pequenas quantidades ao redor do grupo carboxílico da extremidade N-terminal e, cadeias metílicas laterais. Todavia, o comportamento parece não afetar a diferença na estabilidade de equilíbrio conformacional.
Recent papers, both experimental and theoretical, have highlighted the capacity of alcohols and polyalcohol in modifying the energy landscape in proteins. However, the mechanism underlying this effect is not fully elucidated. Taking as a model-system the alanine dipeptide, QM/MM calculations were performed in water, ethanol and solution 60-40% (volume) water-ethanol. The dipeptide molecule was described by MP2/aug-cc-pVDZ level. In solution, only αR and PPII conformers were found in the conformational equilibrium population. The free energy difference in solution αR  PPII is determined by the interplay between internal energy and the interaction energy. It has been found that, for alanine dipeptide, any factor that increases the solute-solvent interaction energy also promotes an increasing on αR stability, moreover factors that decreases this value, such as the addition of ethanol molecules, increases the PPII stability. The results points to a preferential solvation behavior for the system, as evidenced by the composition of the first solvation shell in the mixture mainly populated by water molecules, although it is possible to find small concentration of ethanol molecules around the carboxyl group of the N-terminal end and around methylic side chains. However, this behavior does not seem to affect the differential conformational stability.
CAPES: 99999.014630/2013-03

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Books on the topic "Ethanol Ethanol Opioid peptides"

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(Editor), Judith J. Wurtman, ed. Nutrition and the Brain. Raven Pr, 1990.

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Book chapters on the topic "Ethanol Ethanol Opioid peptides"

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Zhao, Yong-Mei, Xiao-Hong Wang, Shi-Qin Dong, and Shu-Li Sheng. "Protective effect of KA8 peptide on ethanol-induced gastric mucosal erosion in rat." In Peptides, 184–85. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-010-9069-8_48.

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Hoffman, Paula L., Gyula Szabó, and B. Tabakoff. "The effects of vasopressin and related peptides on tolerance to ethanol." In Peptide and Amino Acid Transport Mechanisms in the Central Nervous System, 147–56. London: Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-09927-6_13.

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Méndez, Milagros, Karla Hernández-Fonseca, and Paula Abate. "Prenatal ethanol exposure and enkephalinergic neurotransmission." In Opioid Hormones, 313–37. Elsevier, 2019. http://dx.doi.org/10.1016/bs.vh.2019.05.005.

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"Chemistry in a Nanodrop: From H-Bonds to Peptides." In Computer Based Projects for a Chemistry Curriculum, edited by Thomas J. Manning and Aurora P. Gramatges, 163–82. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/9781608051939113010020.

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In this exercise students will replicate interactions in a simulated solvent (water, ethanol, etc.) drop that have diameters of a few nanometers across. Students will construct systems that will allow them to review some fundamental interactions such as hydrogen bonding, dipole-dipole interactions and ion-dipole interactions. Students will search for correlations or trends involving molecular interactions and physical parameters. Students will look at ionic, atomic and small molecule interactions in a nanodrop of a common solvent such as water, ethanol and methanol. The diameter of these nanodrops typically ranges from two to six nanometers. Students will examine the interaction of a solvent nanodrop with two enkephalin peptides to better understand molecular folding.

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Wyatt, Jonathan P., Robert G. Taylor, Kerstin de Wit, Emily J. Hotton, Robin J. Illingworth, and Colin E. Robertson. "Toxicology." In Oxford Handbook of Emergency Medicine, 187–225. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198784197.003.0004.

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This chapter in the Oxford Handbook of Emergency Medicine encompasses toxicology in the emergency department (ED). It examines poisons in general, including diagnosis, supportive care, reducing absorption, and antidotes. Specific poisoning is explored in detail, through opioid, salicylate, paracetamol, tricyclic antidepressant, benzodiazepine, clomethiazole, phenothiazine, barbiturate, lithium, sulfonylurea, beta-blocker, calcium channel antagonist, digoxin, angiotensin-converting enzyme (ACE) inhibitor, theophylline, salbutamol, iron, ethanol, methanol, ethylene glycol, paraquat, petrol, paraffin, organophosphate, cyanide, carbon monoxide, chlorine, and CS gas (tear gas) poisoning. Chemical incidents are discussed, as well as accidental poisoning from plants, berries, mushrooms, and button batteries. It also examines novel psychoactive substances (NPS), recreational drugs, serotonin syndrome, and body packers.

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K., Carsten, and Selena E. "The Role of Delta Opioid Receptors in Ethanol Consumption and Seeking: Implications for New Treatments for Alcohol Use Disorders." In Neuroscience - Dealing With Frontiers. InTech, 2012. http://dx.doi.org/10.5772/32239.

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Conference papers on the topic "Ethanol Ethanol Opioid peptides"

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Bačová, Zuzana, Lucia Smreková, and Vladimír Štrbák. "Ethanol-induced secretion of TRH in rat heart." In IXth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2005. http://dx.doi.org/10.1135/css200508001.

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Eckhardt, Th, S. Haas, B. Lange, and H. Pfeiffer. "MEASUREMENT OF ELASTASE-INDUCED FIBRINOGEN-DERIVED PEPTIDES IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643165.

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Leukocyte elastase (EL) cleaves peptides from the N-terminal fibrinogen (fbg) Aα and B6 chains. The Aα peptide (Aα 1-21) and the as yet unidentified BIB peptide contain thrombin (TB)cleavage sites. As we were interested in fbg proteolysis in sepsis and leukemia, we have tried to measure these peptides (generated by incubating a crude granulocyte extract with fbg) using available fibrinopeptide A (FPA) - und Bß 15-42-antigen-RIA techniques. As the indirect measurement of Aα 1-21 in terms of FPA releasable by TB treatment in vitro (TB-inducible FPA, TIFPA) requires the use of a highly specific anti-FPA-antiserum to avoid cross reaction of Aα 1-21 we tested the specificity of several antisera. Only R2, provided by Dr. J. Owen, proved suitable whereas two commercial antisera measured 6-15% of Aα 1-21 as apparent FPA. Simultaneous recovery of FPA and Aα 1-21 from plasma using R2 was between 80-100% after precipitation of cross-reacting fbg by ethanol, whereas bentonite adsorbed Aα 1-21 and the EL induced BIB peptide. TIFPA was fully recovered after incubation with plasma (37°C, 2 hr) whereas cross-reactivity of Aα 1-21 in the FPA-assay did not increase. EL-induced proteolysis in plasma in terms of TIFPA generation did not occur unless the normal granulocyte-plasma ratio was increased about 300-400 fold. The Bß 15-42 antigen RIA allowed quantitative measurement of the as yet undefined EL-induced Bß peptide, since the "Bß 15-42" concentration measured was equal to the amount of FPB (measured as Bß 1-13) releasable from the EL-induced BIB-peptide by TB. The immunoreactivity of this peptide is stable in plasma and completely recovered after ethanol precipitation. This finding suggests that the EL-induced BIB peptide is longer than Bß 1-4 2 and not susceptible to C-terminal degradation of the Bß41/42 region which is crucial for recognition of the peptide by the antiserum (supported by Deutsche Forschungs-gemeinschaft).

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Gómez-Carreño, Carlos Rodríguez, Antonio Ramírez García, Luis Beato Fernández, Irene Díaz Quero, and Estefanía Segura Escobar. "Craving and Priming of alcohol in depressive disorders. Bibliographic review and new therapies." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p140.

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Abstract:

Acute alcohol consumption produces positive reinforcement effects, through activation of brain reward circuit, includes limbic system structures (accumbens system and hippocampus). The comorbidity of depressive episode and alcohol abuse makes it necessary to propose new strategies for the treatment of this frequent clinical situation. We conducted a literature review of the combined treatments for major depressive disorder (MDD) with alcohol abuse. We review current literature on the use of new treatments in alcohol consumption with pattern of abuse (binge drinking). Recent studies support the potential clinical importance of NMDA receptor antagonism among the mechanisms underlying the subjective effects of ethanol in humans. The efficacy of medications for alcohol dependence remains modest, and there are no strong clinical predictors of treatment response. We analyze approved medications used today: Acamprosate (NMDA modulator), disulfiram (acetaldehyde dehydrogenase inhibitor), naltrexone (opioid antagonist), nalmefene (opioid antagonist). Promising current studies suggest the glutamatergic pathway and medications such as ketamine could have a hopeful future in the treatment of alcohol use disorder associated with affective disorders.

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