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Relevant bibliographies by topics / Acid peptic disorders

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Academic literature on the topic 'Acid peptic disorders'

Author: Grafiati

Published: 2 June 2025

Last updated: 22 June 2025

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Journal articles on the topic "Acid peptic disorders"

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Kale-Pradhan, Pramodini B., Heather K. Landry, and William T. Sypula. "Esomeprazole for Acid Peptic Disorders." Annals of Pharmacotherapy 36, no. 4 (2002): 655–63. http://dx.doi.org/10.1345/aph.1a104.

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OBJECTIVE: To review the pharmacology, pharmacokinetics, clinical efficacy, and safety of esomeprazole, a new proton-pump inhibitor (PPI). DATA SOURCES: A MEDLINE search (1966–March 2001) was conducted for relevant literature using the terms esomeprazole, Nexium, and H199/18. Abstracts from the XXXII Nordic Meeting of Gastroenterology and journal articles provided by AstraZeneca were reviewed. STUDY SELECTION AND DATA EXTRACTION: All available studies on the pharmacology, pharmacokinetics, clinical efficacy, and safety of esomeprazole were reviewed. DATA SYNTHESIS: Esomeprazole is a new PPI and is the S—isomer of racemic omeprazole. Esomeprazole has demonstrated acid control comparable to that of the other PPIs currently available. Esomeprazole undergoes less hepatic metabolism compared with omeprazole, and thus may result in less interpatient variability among slow and fast metabolizers of CYP2C19. The oral bioavailability of esomeprazole is approximately 89% with a dose of 40 mg, and the half-life is approximately 1.5 hours. Esomeprazole is effective in the healing of erosive esophagitis, with a rate of healing at week 8 of 93.7% (p < 0.001). In maintenance therapy of healed erosive esophagitis, esomeprazole maintained healing rates <90% (6-mo trial). Esomeprazole is comparable with omeprazole (both in combination with appropriate antibiotics) in the eradication of Helicobacter pylori, with eradication rates of 89.7% and 87.8%, respectively. The drug is well tolerated. The few adverse effects associated with esomeprazole are diarrhea, headache, nausea, abdominal pain, respiratory infection, and sinusitis. CONCLUSIONS: Esomeprazole is a safe and effective PPI. It is effective in the treatment of peptic ulcer disease and gastroesophageal reflux disease.

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Kuwayama, Hajime. "ADVANCES IN TREATING ACID PEPTIC DISORDERS." Journal of Gastroenterology and Hepatology 15, no. 12 (2000): H31. http://dx.doi.org/10.1046/j.1440-1746.2000.015012h31.x.

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Nasir, M., and AFM M. Rahman. "Proton Pump Inhibitors : The Controversies to Consider." Journal of Medical Science & Research 19, Number 2 (2012): 33–37. http://dx.doi.org/10.47648/jmsr.2012.v1902.06.

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Heartburn is ailing the masses. By one estimate. 20% of the Western population experiences acid reflux at least once a week and shelling out buckets of cash S25.6 billion worldwide in 2008 to alleviate those hot, sour. acidic pains in the chest. Proton pump inhibitors (PPIs) am one of the most commonly prescribed classes of medications in the primary care setting and are considered a major advance in the treatment of acid-peptic diseases. Since the introduction of omeprazok in 1989. several other PPIs have become available in combating various acid-peptic disorders, including gastroesophageal reflux disease, peptic ulcer disease, and nonsteroidal anti-inflammatory drug-induced gastropathy. The intravenous form of pantoprazole is now available. and the U.S. Food and Drug Administration (FDA) approved the newest dexlansoprazole in 2012. Although H2 blockers are less expensive thanPPIs, but PPIs provide superior acidsuppression, healing rates and symptom relief.Therefore, PPIs may be more cost-effectivethan H2 blockers. especially in patients withmore severe acid-peptic disorders, because oftheir lower and less frequent dosingrequirements and their comparatively shorterduration of required therapy.

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Nasir, M., and AFM M. Rahman. "Proton Pump Inhibitors : The Controversies to Consider." Journal of Medical Science & Research 19, Number 2 (2012): 33–37. http://dx.doi.org/10.47648/jmsr.2012.v1902.07.

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Heartburn is ailing the masses. By one estimate. 20% of the Western population experiences acid reflux at least once a week and shelling out buckets of cash S25.6 billion worldwide in 2008 to alleviate those hot, sour. acidic pains in the chest. Proton pump inhibitors (PPIs) am one of the most commonly prescribed classes of medications in the primary care setting and are considered a major advance in the treatment of acid-peptic diseases. Since the introduction of omeprazok in 1989. several other PPIs have become available in combating various acid-peptic disorders, including gastroesophageal reflux disease, peptic ulcer disease, and nonsteroidal anti-inflammatory drug-induced gastropathy. The intravenous form of pantoprazole is now available. and the U.S. Food and Drug Administration (FDA) approved the newest dexlansoprazole in 2012. Although H2 blockers are less expensive thanPPIs, but PPIs provide superior acidsuppression, healing rates and symptom relief.Therefore, PPIs may be more cost-effectivethan H2 blockers. especially in patients withmore severe acid-peptic disorders, because oftheir lower and less frequent dosingrequirements and their comparatively shorterduration of required therapy.

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Gustavsson, S., and L. Engstrand. "Future Strategies in Acid-peptic Disorders: Concluding Remarks." Scandinavian Journal of Gastroenterology 23, sup142 (1988): 114–16. http://dx.doi.org/10.3109/00365528809091725.

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Saltiel, Emmanuel. "Peptic Acid Disorders: Developing a Disease Management Program." Journal of Managed Care Pharmacy 2, no. 5 (1996): 569–75. http://dx.doi.org/10.18553/jmcp.1996.2.5.569.

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Parthasarathy, Srinivasan. "Vonoprazan – A New Drug for Acid Peptic Disorders." SBV Journal of Basic, Clinical and Applied Health Science 7, no. 3 (2024): 103–4. http://dx.doi.org/10.4103/sbvj.sbvj_42_24.

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CLEARFIELD, H. R. "Challenges in acid/peptic disorders: a symposium overview." Alimentary Pharmacology & Therapeutics 5 (March 31, 2007): 1–4. http://dx.doi.org/10.1111/j.1365-2036.1991.tb00743.x.

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LEWIS, J. H. "Idiopathic gastric acid hypersecretion: treatment implications for refractory acid/peptic disorders." Alimentary Pharmacology & Therapeutics 5 (March 31, 2007): 15–24. http://dx.doi.org/10.1111/j.1365-2036.1991.tb00745.x.

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Islam, M. M. Shahin Ul. "“Potassium Competitive Acid Blocker”- new Weapon to Combat Acid Peptic Disorders." Bangabandhu Sheikh Mujib Medical College Journal 2, no. 2 (2023): 72–73. http://dx.doi.org/10.3329/bsmmcj.v2i2.69830.

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Dissertations / Theses on the topic "Acid peptic disorders"

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Minnie, Jacqueline Louise. "An education intervention on prescribing patterns of drugs for acid-related disorders in a clinic setting : a case study / Jacqueline Louise Minnie." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1562.

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Janse, van Rensburg Hendrika Nicolien. "A longitudinal study of the usage of acid reducing medicine using a medicine claims database / Hendrika Nicolien Janse van Rensburg." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1903.

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Acid-related disorders are common, chronic conditions that have considerable impact on a patient's quality of life. In a study conducted by Majumdar et al. (2003:2411) the prevalence of chronic acid-related disorders was 2.3%. Acid-related disorders represent a major financial consideration with respect to the costs of drug prescribing (Whitaker, 1998:6). Health care cost increases each year. This leads to an increased interest in economic evaluation of health care and medical technologies (Anell & Svarvar, 2000:175). Health care providers no longer make treatment decisions independent of the consideration of the resultant cost. The treatment provided must not only provide value but the value must be documented to justify spending money. Economic evaluation research has emerged to offer guidance to policy makers, practitioners, health plans and institutions facing difficult treatment and coverage decisions (Ellis era/., 2002:271). The main objectives of this study were to investigate the prescribing patterns and cost of acid reducing medicine with special reference to proton pump inhibitors and histamine-2 receptor antagonists in a section of the private health care sector of South Africa from 2001 to 2006. A longitudinal retrospective drug utilisation study was done on acid reducing medicine items claimed through a national medicine claims database. The five study years were 2001, 2002, 2004, 2005 and 2006. All the study years stretched from 1 January to 31 December. It was determined that acid reducing medicine items prescribed decreased from 2.74% during 2001 to 2.50% during 2006 of all medicine items claimed. The same decreasing trend was observed regarding the cost of acid reducing medicine items. The cost percentage decreased from 4.89% (2001) to 3.72% (2006). However, the average cost per medicine item for the acid reducers increased by 5.35% from 2001 (R230.04 ± 176.29) to 2002 (R243.72 ± 184.18) and then decreased by 15.23% from 2002 to 2004. It again decreased with 15.05% from 2004 (R206.19 ± 179.42) to 2006 (R175.70 ± 172.55). The changes in the average cost of acid reducers were of no practical significance. Proton pump inhibitors represented about half of the acid reducing medicine items prescribed and more than 70% of the total cost of acid reducing medicine items during the study years. The average cost of PPIs revealed a practical significant decrease (d > 0.8) from 2002 (R372.42 ± 156.62) to 2006 (R241.56 ± 177.21). H2RAs contributed between 15.00% and 18.26% of all acid reducing medicine items while contributing to between 9.68% and 16.85% of the total cost of all acid reducers. The active ingredient most often prescribed was lansoprazole during 2001 and 2002, esomeprazole during 2004 and omeprazole during 2005 and 2006. Lanzor® 30mg was the acid reducer with the highest cost from 2001 to 2005, while Pariet® 20mg took the lead in 2006. Zantac® 150mg effervescent tablets were the H2RA, with the highest cost, during the five study years. The percentage innovator items decreased by 4.50% from 2001 to 2002, increased by 1.01% from 2002 to 2004 and decreased again by 31.06% from 2004 to 2006. The slight increase in the percentage innovator medicine items claimed from 2002 to 2004 may be explained by the introduction of Nexiam® (esomeprazole) into the market in 2002. The total number of generic medicine items claimed contributed between 9.62% (n = R1 788 242.25) in 2001 and 30.75% (n = R3 196 163.34) in 2006 of the total cost of acid reducing medicine items. The average cost per day of innovator medicine items was higher than the average cost per day of generic medicine items. This might be explained by a lower average cost for generic medicine items. It was also determined that the prevalence of the two-drug regimens was the highest during the five study years. The Helicobacter pylori (H.pylori) eradication treatments, which included different antibiotics, increased from 2.72% in 2001 to 5.05% in 2006. The PDD for most of the active ingredients of H2RAs and PPIs remained stable during the study years. However, it appears that the PDDs, of the PPIs, active ingredients were more constant than the PDDs, or the H2RAs, active ingredients. The median of the different PPI active ingredients was reasonably more constant than the median of the different H2RA active ingredients. Thus the changes between the PPIs' and H2RAs' active ingredients might be explained by the variation in the median (the number of days the relevant medicine item was claimed for). It is then also recommended that the aspects of generic substitution as well as the usage of H2RAs as prescribed vs. self medication should be further investigated to increase possible cost savings.<br>Thesis (M.Pharm. (Pharmacy Practice))--North-West University, Potchefstroom Campus, 2008.

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Ramraj, Varun. "Exploiting whole-PDB analysis in novel bioinformatics applications." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:6c59c813-2a4c-440c-940b-d334c02dd075.

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The Protein Data Bank (PDB) is the definitive electronic repository for experimentally-derived protein structures, composed mainly of those determined by X-ray crystallography. Approximately 200 new structures are added weekly to the PDB, and at the time of writing, it contains approximately 97,000 structures. This represents an expanding wealth of high-quality information but there seem to be few bioinformatics tools that consider and analyse these data as an ensemble. This thesis explores the development of three efficient, fast algorithms and software implementations to study protein structure using the entire PDB. The first project is a crystal-form matching tool that takes a unit cell and quickly (< 1 second) retrieves the most related matches from the PDB. The unit cell matches are combined with sequence alignments using a novel Family Clustering Algorithm to display the results in a user-friendly way. The software tool, Nearest-cell, has been incorporated into the X-ray data collection pipeline at the Diamond Light Source, and is also available as a public web service. The bulk of the thesis is devoted to the study and prediction of protein disorder. Initially, trying to update and extend an existing predictor, RONN, the limitations of the method were exposed and a novel predictor (called MoreRONN) was developed that incorporates a novel sequence-based clustering approach to disorder data inferred from the PDB and DisProt. MoreRONN is now clearly the best-in-class disorder predictor and will soon be offered as a public web service. The third project explores the development of a clustering algorithm for protein structural fragments that can work on the scale of the whole PDB. While protein structures have long been clustered into loose families, there has to date been no comprehensive analytical clustering of short (~6 residue) fragments. A novel fragment clustering tool was built that is now leading to a public database of fragment families and representative structural fragments that should prove extremely helpful for both basic understanding and experimentation. Together, these three projects exemplify how cutting-edge computational approaches applied to extensive protein structure libraries can provide user-friendly tools that address critical everyday issues for structural biologists.

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Van, Rensburg Hendrika Nicolien Janse. "A longitudinal study of the usage of acid reducing medicine using a medicine claims database / H.N. Janse van Rensburg." Thesis, 2007. http://hdl.handle.net/10394/1903.

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Books on the topic "Acid peptic disorders"

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Arnold, Berstad, ed. Management of peptic ulcer disease and acid-related disorders: Clinical aspects of antacids in the 1990s : Bermuda, November 15-16, 1991. Raven Press, 1992.

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2

Peptic ulcer disease and other acid-related disorders. Academic Research Associates, 1991.

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3

Clearfield, Harris R. Acid-Peptic Disorders of the Upper Gastrointestinal Tract: Diagnosis and Management. Handbooks in Health Care, 1995.

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4

Freston, James W. Diseases of the Gastroesophageal Mucosa: The Acid-Related Disorders. Humana Press, 2012.

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Freston, James W. Diseases of the Gastroesophageal Mucosa: The Acid-Related Disorders. Humana Press, 2001.

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6

(Editor), Henry Parkman, and Robert S. Fisher (Editor), eds. The Clinician's Guide to Acid/Peptic Disorders and Motility Disorders of the Gastrointestinal Tract (The Clinician's Guide to GI Series). Slack Incorporated, 2006.

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Modlin, Irvin M., and George Sachs. Acid Related Diseases: Biology and Treatment. 2nd ed. Lippincott Williams & Wilkins, 2004.

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Sedlack, Robert E., Conor G. Loftus, Amy S. Oxentenko, and Thomas R. Viggiano. Gastroenterology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0210.

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Part 1 reviews the major portions of the gastrointestinal system (esophagus, stomach, small intestine, colon, and pancreas), their function (motility, acid production, enzymatic function, and absorption), and various disorders associated with them (dysmotility, ulceration, malabsorption, inflammation, and dysplasia). Symptoms, diagnostic testing, and treatment of common gastrointestinal conditions, such as gastroesophageal reflux disease, peptic ulcer disease, diarrhea, constipation, inflammatory bowel disease, and pancreatitis, are reviewed.

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.

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Book chapters on the topic "Acid peptic disorders"

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Kovacs, Thomas O. G. "Acid-Peptic Disorders." In Gut Instincts. CRC Press, 2024. http://dx.doi.org/10.1201/9781003524489-11.

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Lakshmanan, Mageshwaran. "Drugs Used in Acid Peptic Disorders." In Introduction to Basics of Pharmacology and Toxicology. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6009-9_34.

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"Acid Peptic Disorders." In Yamada's Handbook of Gastroenterology. John Wiley & Sons, 2013. http://dx.doi.org/10.1002/9781118572610.ch21.

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Qadeer, Mohammed A., and Gary W. Falk. "Acid Peptic Disorders." In Current Clinical Medicine. Elsevier, 2010. http://dx.doi.org/10.1016/b978-1-4160-6643-9.00065-5.

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Daneshmend, Tawfique, and Alasdair Dow. "Gastroenterological disorders." In Perioperative Medicine. Oxford University PressOxford, 2006. http://dx.doi.org/10.1093/oso/9780199211739.003.0030.

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Abstract A history of acid-peptic ulceration of the upper digestive tract affecting the duodenum, stomach, or oesophagus will often be obtained in patients presenting for elective or emergency surgery unrelated to the upper GI tract. Surgery for acid-peptic disease itself (elective surgery for peptic ulcer, gastro-oesophageal reflux disease; emergency surgery for perforated peptic ulcer or oesophagus; or surgery for acute GI bleeding) is not the purpose of this chapter. The management of these patients is addressed in standard surgical texts. Chronic peptic ulceration should now be rare. Since over 90% of (previously idiopathic) gastric and duodenal ulceration is associated causally with Helicobacter pylori, in ideal circumstances previous eradication of this bacterium should have eliminated the need for continuing medical therapy.

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Vikraman Pillai, R. "Acid Peptic Disease." In PG Textbook of Pediatrics: Infections and Systemic Disorders (Volume 2). Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12854_100.

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"Gastric Physiology and Acid-Peptic Disorders." In Modern Surgical Care. CRC Press, 2006. http://dx.doi.org/10.3109/9781420016581-19.

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Boarder, Michael, Jane Dixon, David Newby, Phyllis Navti, and Tyra Zetterström. "Upper gastrointestinal tract disorders." In Pharmacology for Pharmacy and the Health Sciences. Oxford University Press, 2016. http://dx.doi.org/10.1093/9780198728832.003.0012.

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This chapter focuses on upper gastrointestinal tract disorders. The commonly experienced symptoms of heartburn, acid regurgitation, and indigestion (dyspepsia) arise from disturbances of acid secretion in the stomach and the consequent damage to the mucosal lining of the oesophagus, stomach, or duodenum. Conditions affecting the upper gastrointestinal tract, like gastro-oesophageal reflux disease and peptic ulcer disease, are among the most prevalent illnesses in Western countries. The chapter discusses the causes and significance of nausea and vomiting. It cites that the main targets for antiemetic therapy are receptors in the chemoreceptor trigger zone (CTZ) and those involved in the pathways to the emesis centre.

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Aridome, Kuniaki. "Benign diseases of the stomach." In Oesophagus and Stomach, edited by Matthias Reeh, Jakob R. Izbicki, Samiran Nundy, and Dirk J. Gouma. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780192863591.003.0005.

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Abstract Most benign diseases of the stomach are attributed to functional dyspepsia and acid-related disorders such as peptic ulcer disease. Dyspepsia is also the main manifestation of these acid-related conditions of the stomach. Functional dyspepsia comprises three subtypes: postprandial distress syndrome, epigastric pain syndrome, and a subtype with overlapping postprandial distress syndrome and epigastric pain syndrome features. Peptic ulcer disease is characterized by a non-malignant lesion in the gastrointestinal mucosa that may be acute, subacute, or chronic. Proton pump inhibitors significantly improve the management options available for patients with functional dyspepsia or peptic ulcer disease. Reduction of inappropriate prescribing of proton pump inhibitors in inpatient and outpatient settings can minimize the potential for adverse events.

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Garg, Dr Gopal. "Antiulcer Agents." In Edited Book of Pharmacology-III [According to Latest Syllabus of B. Pharm-VI Semester of Pharmacy Council of India]. Iterative International Publishers, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/nbennurphch2.

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Antiulcer agents are essential medications used to manage and treat conditions like peptic ulcers, gastroesophageal reflux disease (GERD), and other acid-related disorders of the gastrointestinal tract. These agents are classified into several categories based on their mechanisms of action: proton pump inhibitors (PPIs), H2-receptor antagonists (H2RAs), antacids, mucosal protective agents, antibiotics, and prostaglandin analogues. PPIs, such as omeprazole and lansoprazole, work by irreversibly inhibiting the hydrogen-potassium ATPase enzyme, significantly reducing gastric acid secretion. H2RAs, including ranitidine and famotidine, competitively inhibit histamine at H2 receptors, decreasing acid production. Antacids like magnesium hydroxide and calcium carbonate neutralize stomach acid, providing rapid symptomatic relief. Mucosal protective agents, such as sucralfate and bismuth subsalicylate, protect the gastric lining by forming a barrier or coating ulcers. Antibiotics like clarithromycin and amoxicillin are used in combination regimens to eradicate Helicobacter pylori, a common cause of peptic ulcers. Prostaglandin analogues, like misoprostol, enhance mucosal defenses by increasing mucus and bicarbonate secretion. Each of these agents has specific therapeutic uses and potential side effects, making them integral to the effective management of acid-related gastrointestinal conditions.

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Conference papers on the topic "Acid peptic disorders"

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Bauer, K. A., B. L. Kass, M. Bednarek, M. Kloczewiak, J. Hawiger, and R. D. Rosenberg. "DETECTION OF FACTOR X ACTIVATION IN HUMANS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643828.

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The activation of factor X by factor VII/VIIa-tissue factor or factor IXa plays a pivotal role in the hemostatic mechanism. This reaction results in the liberation of a peptide from the zymogen for which we have developed a sensitive and specific radioimmunoassay (RIA), The native peptide was purified from activated human factor X by hydroxylapatite chromatography and reverse-phase high pressure liquid chromatography (HPLC). Gel filtration experiments demonstrated that the peptide was not physically associated with the enzyme. A 15 amino acid peptide with the COOH-terminal sequence of the activation fragment was synthesized using the solid-phase method of Merrifield. Antisera were raised in rabbits to the synthetic analogue coupled to bovine serum albumin with glutaraldehyde. The antibody population obtained was used to construct a double antibody RIA and was able to measure as little as 0.02 nM of this component. The antibody reactivity toward the factor X zymogen was negligible (less than 1/36,000 that of the activation peptide on a molar basis). However because other plasma constituents contributed to a nonspecific basal signal in the RIA, we developed an extraction procedure for the native peptide utilizing perchloric acid. Plasma peptide levels in normal individuals were ∼0.1 nM, and elevations up to 0.8 nM were observed in patients with evidence of disseminated intravascular coagulation. Individuals chronically anticoagulated with coumarin derivatives had plasma levels of this peptide suppressed to ∼0.02 nM. The validity of our measurements of factor X activation in vivo is supported by the fact that the immunoreactive signal migrates on reverse-phase HPLC in a manner identical to that of the native activation peptide and can be quantitatively recovered. This assay should be useful for studying the pathophysiology of thrombotic as well as bleeding disorders in humans.

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Kibitkina, A. A., E. R. Vasilevskaya, N. A. Ilin, and G. S. Tolmacheva. "CHANGES IN MILK OF TPH2 HET MICE UNDER EXPOSURE TO STRESS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. LLC Institute Information Technologies, 2024. http://dx.doi.org/10.47501/978-5-6044060-4-5.41-46.

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The relationship between neuroregulatory factors of the brain and the composition of breast milk is an interesting and little-studied topic. The article is aimed at studying changes in the chemical composition of the milk of mice prone to the development of affective disorders (heterozygous for TPH2) under the influence of stress and without stress relative to the milk of ordinary mice. Raman spectroscopy (wavelength 785 nm, focal length 50x) was used for the study. Het mouse milk has a less rich protein and peptide profile, but the range of fatty acids, especially under stress, increases.

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Müller, E., and A. Henschen. "HUMAN PLASMA FIBRINOGEN MOLECULAR WEIGHT VARIANTS:CHARACTERIZATION BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY AND IDENTIFICATION BY SEQUENCE ANALYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643328.

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Human plasma has been shown to contain several fibrinogen variants which differ from each other in molecular weight. The three most common forms, with molecular weights of 340 kD, 305 kD and 270 kD, have been reported to change considerably in their relative amounts during certain pathophysiological processes such as acute phase reactions, disseminated intravascular coagulation, fibrinolytic disorders, liver disease and cancer. Though it has been suggested that the differences in molecular weight are due to degradation of one or both, respectively, of the carboxy-terminal parts of the Aα-chains, the removed or altered segments have so far never been precisely determined. Consequently, it has only been possible to speculate about the origin of the variants.The aim of this study was to isolate the various molecular weight variants from plasma and to characterize their peptide chain components proteinchemically. Fibrinogen was first isolated from plasma by glycin precipitation and the variants were then separated by stepwise ammonium sulfate precipitation, taking advantage of their different solubility.The peptide chain components of the various fractions were isolated by reversed-phase high-performance liquid chromatography (HPLC). The N-termini were identified by direct sequence analysis. Chemical and enzymatic cleavages of the peptide chains resulted in fragment mixtures which were compared with the corresponding mixtures obtained from commercial fibrinogen by HPLC fingerprinting. Finally, the fragments which differed were identified by N-terminal sequence and amino acid analysis so that the exact C-termini of the peptide chains,especially in the lower molecular weight variants,could be determined. With the help of this information conclusions may also be drawn about the origin of the lower molecular weight variants and about the mechanism by which they may he formed.

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Lazarević, Marija. "COGNITIVE, HEMATOPOIETIC AND GASTROINTESTINAL IMPAIRMENTS CAUSED BY VITAMIN B12 DEFICIENCY – PATOGENESIS, TREATMENT AND PATIENT CARE." In Global Challenges Through the Prism of Rural Development in the Sector of Agriculture and Tourism GIRR 2024. Academy of Applied Studies Šabac, 2025. https://doi.org/10.46793/girr25.287l.

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Many studies have investigated the pathogenetic association of cognitive, hematopoietic, and gastrointestinal impairments with low vitamin B12 concentrations. The aim of our study is to point out the importance of maintaining vitamin B12 concentrations in the body, in order to preserve cognition, but also other vital parameters of the body. For a systematic literature search on studies on the association of cognitive, hematopoietic and gastrointestinal impairments with vitamin B12 deficiency, we used we used the databases: Web of Science, PubMed, Google Scholar. The search keywords included “vitamin B12“, “cognition“, “anemia“ and “gastrointestinal diseases“. Vitamin B12 deficiency can lead to cognitive disorders and dementia in addition to hematological and gastrointestinal symptoms. This can occur due to insufficient intake, inadequate absorption or its reduced utilization. Vitamin B12 is involved in myelin repair, amino acid metabolism, and bone marrow cell production. If there is a vitamin B12 deficiency in the body, symptoms usually first appear in the gastrointestinal tract. Due to the lack of intrinsic factor and the presence of autoantibodies against gastric parietal cells or intrinsic factor, vitamin B12 absorption disorders and pernicious anemia occur. After gastrectomy, but also after removal of the distal ileum or the presence of tumors that interfere with absorption, achlorhydria and pepsin deficiency occur, which causes vitamin B12 deficiency and megaloblastic anemia. Due to the lack of vitamin B12 in the body, significant damage can occur and its compensation through supplementation is necessary. Therefore, it is necessary to determine this deficiency in a timely manner in order to prevent its consequences, which may be irreversible.

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Askew, Michael J., Gary B. Schneider, Kristina J. Grecco, Jason Hsu, Emily Mugler, and Donald A. Noe. "Effect of Pharmaceutical Bone Growth Stimulation With Novel Anabolic Peptides: Biomechanical and Bone Density Measurements in a Rat Model." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43044.

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Pharmaceutical bone growth stimulation holds promise for prevention and treatment bone disorders, and the enhancement of fracture healing. Bone growth hormones have begun to have limited clinical use, but can illicit adverse side effects. Recent studies have shown that short peptides (less than 15 amino acids) derived from the protein sequence of Vitamin D Binding Protein (DBP), can enhance bone formation (osteogenesis). These peptides may have potential as controllable bone growth stimulators without the adverse side effects and cost of bone growth hormones. Rats, injected every other day for two weeks with DBP-based peptide fragments ranging from 3 to 13 amino acids in length, were euthanized and the tibias and femurs were scanned by peripheral quantitative computerized tomography (pQCT) to determine bone density and cross-sectional geometric properties. The bones were then tested in three-point bending to determine strength and bending modulus. Injection of DBP-based peptides over only a 2-week period resulted in significant (p&lt;0.05) increases in bone density and material properties in the experimental rat bones in comparison to controls injected with saline. The short length of these effective peptides suggests their use not only in systemic injections but also as clinically convenient pills taken orally for pharmaceutically induced bone growth stimulation.

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Scheefers-Borchel, U., and G. Muller-Berghaus. "A NEW FIBRIN-SPECIFIC ANTIBODY DISCRIMINATING BETWEEN FIBRIN AND FIBRINOGEN IS DIRECTED AGAINST THE SYNTHETIC PEPTIDE LEU-ILE-ASP-GLY-LYS-MET." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643771.

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To determine soluble fibrin in blood of patients with coagulation disorders we produced monoclonal antibodies which distinct fibrin from fibrinogen and other blood constituents. Fibrin-specific monoclonal antibodies were obtained by immunizing mice with the synthetic hexapeptide Leu-Ile-Asp-Gly-Lys-Met which was covalently linked to KLH via its C-terminus. Several of the monoclonal antibodies which reacted with the hexapeptide also reacted with batroxobin-induced desAA-fibrin and thrombin-induced desAABB-fibrin, but not with fibrinogen. No reaction was observed with plasmin-induced fibrinogenolytic and fibrinolytic degradation products, respectively. The epitope recognized by these fibrin-specific antibodies is located on the αchain of fibrin and is not accessible for an antibody in native fibrinogen. One monoclonal antibody (B/H11) was used to quantify the amount of soluble fibrin in plasma of patients with a variety of coagulation disorders. This antibody could also be used to develop an ELISA based on two different fibrin-specific monoclonal antibodies. For this assay anti-fbn 17 (Scheefers- Borchel et al., Proc. Natl. Acad. Sci. USA 82: 7091, 1985) was coated onto ELISA plates. After adding plasma which contained soluble fibrin, the fibrin bound was detected by the second fibrin-specific antibody B/H^ to which biotin was covalently linked. The second antibody was probed by the addition of peroxydase conjugated streptavidin and the substrate ABTS for peroxydase. This test can be used to detect fibrin at concentrations as low as 70 ng/ml. With this assay system, it is possible to measure the amount of soluble fibrin present in plasma samples without the interference of fibrinogen which is associated with soluble fibrin.

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Homes, W. E., H. R. Lijnen, L. Nelles, C. Kluft та D. Collen. "AN ALANINE INSERTION IN α2-ANTIPLASMIN ‘ENSCHEDE’ ABOLISHES ITS PLASM IN INHIBITORY ACTIVITY". У XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642897.

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Congenital deficiencies of the fibrinolytic inhibitor α2antiplasmin (α2AP) may result in bleeding disorders. An abnormal a AP (α2AP‘Enschede’) is known. 2 siblings with 3% functional activity and normal antigen level have parents with 50% activity and normal antigen. The protein interacts normally with the lysine-binding site(s) of plasmin(ogen) but does not inhibit plasmin irreversibly. α2AP Enschede is a plasmin substrate that like the normal protein releases a M 8,000 peptide upon reaction with plasmin. In the present study, Southern blot analysis, using an α2AP cDNA probe showed a restriction fragment length polymorphism within a small genomic DNA fragment of the Enschede family members. Cloning and sequencing of these fragments revealed a GCG inframe insertion that results in an alanine addition between amino acids 353 and 357, 7-10 positions NH -terminal to the reactive site PI residue, Arg364. This area is homologous to the A4 B-sheet of reactive site cleaved a -antitrypsin. Clones from each individual confirm the parents as true heterozygotes and the children as true homozygotes. A cloned genomic DNA sequence containing the insertion (V ) was exchanged for the normal sequence in a eukaryotic a AP expression plasmid. Recombinant α2AP‘Enschede’ (ra AfVAla) purified from the conditioned media of transfected Chinese Hamster Ovary Cells is analogous to plasma a α2AP‘Enschede’ with respect to interactions with plasmin and plasminogen. Preliminary analysis of the released Mr 8,000 recombinant peptide shows that its NH -terminus is the same as the peptide cleaved from normal a AP. Although ra α2APVAla does not inhibit plasmin irreversibly it does, however, act as a competitive inhibitor of hydrolysis of the chromogenic substrate S-2251 by plasmin.The K for this interaction is 25 nM. Thus, α2APAla retains a high affinity for the active center of plasmin. In conclusion, an Ala insertion near the reactive site of α2AP must have resulted in a structural perturbation that has abolished the plasmin inhibitory activity of a α2AP‘Enschede’. This variant may provide a model for further investigation of structure-function relationships in the serpins which determine the relative inhibitor vs. substrate properties.

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Asen, Nancy, and Rotimi Aluko. "Functional Properties of Enzymatic Pea Protein Hydrolysates That Inhibit in vitro Activities of Acetylcholinesterase and Butyrylcholinesterase." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/ktht4252.

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Overview: Alzheimer’s disease (AD) is a neurodegenerative disorder prevalent among the aged population with morbidity and mortality rate of ~ 12%. Research has linked the cause of this disorder to the loss of acetylcholine through excessive activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Therefore, a promising therapeutic approach for AD treatment is the inhibition of AChE/BChE activities. Common features of an AD brain include low levels of acetylcholine, the presence of amyloid-β peptides deposits and severe oxidative stress triggered by lipid peroxidation and formation of free radicals. Natural peptides that possess antioxidant and bioactivities could have prospects for use in AD management. Objectives: Optimize enzymatic hydrolysis of yellow field pea proteins into protein hydrolysates that possess antioxidant, anti-AChE and anti-BChE activities. Methods: Pea protein (70%) was hydrolyzed using six as alcalase (AH), chymotrypsin (CHH), flavourzyme (FZH), pancreatin (PCH), pepsin (PEH) and trypsin (TPH). The supernatants were sequentially passed through ultrafiltration (UF) membranes with molecular weight cut-off of 1, 3, 5 and 10 kDa to collect the permeates as < 1, 1-3, 3-5, and 5-10 kDa, respectively. The hydrolysates and UF fractions were screened for inhibition of linoleic acid peroxidation (LAP) in addition to radical scavenging (hydroxyl and superoxide) and anti-AChE/BChE properties.Results: Hydrolysates showed varying degrees of radicals scavenging and LAP, as well as anti-AChE and anti-BChE activities but the potency improved by >10% for most UF fractions. AH, FZH, PEH and the UF fractions (1-3 kDa) exhibited better and statistically significant (p<0.05) radical scavenging and AChE/BChE activities than other hydrolysates by 20-30% and 20-40% respectively at same concentrations (10-50 µg).Significance of study: The results suggest that pea protein-derived peptides could be potential candidates for use in the inhibition of AChE and BChE activities, which could provide therapeutic tools suitable for the prevention and treatment of AD.

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Antonarakis, E. "The Molecular Genetics of Hemophilia A Stylianos." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643980.

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Hemophilia A is a common X linked hereditary disorder of blood coagulation due to deficiency of factor 8. The gene for factor 8 has been cloned and characterized (Nature 312:326-342, 1984). It is divided into 26 exons and 25 introns and spans 186 kb of DNA. The CGNA is 9 kb and codes for 2351 amino acids. The first 19 amino acids comprise the secretory leader peptide and the mature excreted polypeptide consists of 2332 amino acids. The nucleotide sequence of the exons and the exon-intron junctions is known and the complete amino acid sequence has been deducedSeveral laboratories have used cloned factor 8 DNA sequences as probes to characterized mutations that are responsible for hemophilia A in certain pedigrees. These mutations have been characterized by restriction analysis, oligonucleotide hybridization, cloning and sequencing of DNA from appropriate patientsIn about 500 patients with hemophilia A examined, the molecular defect has been recognized in 39. Both gross alterations (mainly deletions) and point mutations of the factor 8 gene have been found.A total of 19 different deletions have been observed. No two unrelated pedigrees share the same exact deletion.The size of the deleted DNA varies from 1.5 kb to more than 210 kb. All but one of these deletions are associated with severe hemophilia A. A deletion of 6 kb that contains exon 22 only is associated with moderate hemophilia. Some deletions are present in patients with inhibitors to factor 8. No correlation of the size or the position of the deletions can be found with the presence of inhibitors to factor 8.A total of 20 point mutations have been characterized. All are recognized by restriction analysis and involve Taq I sites. All are mutations of CpG dinucleotides and generate nonsense or missence codons. Unrelated pedigrees have the same single nucleotide change because of independent origin of the same mutation. In many instances de novo occurrence of a point mutation has been observed. CpG dinucleotides are hot spots for mutation to TG or CA presumably because of spontaneous deamination of methylcytosine. Some point mutations are present in patients with inhibitors but no correlation of the site of mutation and inhibitor formation has been found. The nonsense mutations are present in patients with severe hemophilia A. A missense mutation (Arg Gin) in exon 26 was found in a patient with mild hemophilia while another Arg Gin mutation in exon 24 has been observed in a patient with severe disease. The creation of a donor splice site in IVS 4 of factor 8 gene has been observed in a patient with mild hemophilia.Few DNA polymorphisms within the factor 8 gene and two other closely linked polymorphisms have been used for carrier detection and prenatal diagnosis of hemophilia A. These DNA markers are useful in more than 90% of families at risk for hemophilia A.The author thanks Drs. Gitschier, Din, Olek, Pirastou, Lawn for communication of their data prior to publication.The hemophilia project at Johns Hopkins was supported by an Institutional grant and NIH grant to S.S.A. and Haig H. Kazazian, Jr.

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