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Статті в журналах з теми "Pathogenesis"

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Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 29 липня 2024

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1

Orazov, M. R., V. E. Radzinsky, E. D. Dolgov, and Yu G. Abramashvili. "Pathogenesis and pathogenetic options in endometriosis management." Voprosy ginekologii, akušerstva i perinatologii 22, no. 1 (2023): 92–104. http://dx.doi.org/10.20953/1726-1678-2023-1-92-104.

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This article provides a literature review on the etiopathogenesis of endometriosis. Particular attention was paid to genetic and molecular biological aspects of endometriosis. The issues of conservative management of patients with confirmed endometriosis were also considered. The use of dienogest in the treatment of patients with endometriosis was substantiated. Key words: endometriosis, etiopathogenesis, genetic and molecular determinants, dienogest

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2

Tanashyan, M. M., K. V. Antonova, N. E. Spryshkov, A. А. Panina, O. V. Lagoda, and E. P. Shchukina. "Diabetic Polyneuropathy: from Pathogenesis to Pathogenetic Therapy." Effective Pharmacotherapy 20, no. 8 (June 21, 2024): 54–62. http://dx.doi.org/10.33978/2307-3586-2024-20-8-54-62.

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The growing worldwide prevalence of prediabetes and diabetes mellitus (DM) has led to an increase in the incidence of related chronic complications, the most common of which is diabetic polyneuropathy (DPN). The development of DPN is caused by chronic hyperglycemia and potentially modifiable cardiovascular risk factors, including elevated triglyceride levels, body mass index, smoking and hypertension. Social determinants of health are also risk factors for DPN. The review presents data on the pathophysiology of DPN with consideration of the causes of the sequence of symptoms. Discussed the mechanisms and significance of mitochondrial damage, metabolic disorders and regulatory functions of Schwann cells, and issues of autophagy. Noted the role of factors such as hyperglycemia, dyslipidemia, insulin resistance and microvascular disorders, described the signaling pathways and epigenetic changes associated with DPN. Emphasized the role of lifestyle changes and behavioral interventions in the comprehensive management of patients with lesions of the peripheral nervous system in DM. Highlighted modern approaches to the treatment of diabetic neuropathy from the point of view of the mechanisms leading to its progression, as well as unresolved issues and prospects are outlined.

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3

Roy, Saumendu Deb. "Pathogenesis of COVID-19." INDIAN RESEARCH JOURNAL OF PHARMACY AND SCIENCE 7, no. 4 (September 2020): 2354–58. http://dx.doi.org/10.21276/irjps.2020.7.3.3.

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4

Strokov, I. A., and V. V. Oganov. "Pathogenesis, evaluation and pathogenetic therapy of diabetic polyneuropathy." Neurology, Neuropsychiatry, Psychosomatics 13, no. 3 (June 24, 2021): 99–106. http://dx.doi.org/10.14412/2074-2711-2021-3-99-106.

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The increase in the number and life expectancy of patients with diabetes mellitus (DM) worldwide determines the high prevalence of late complications of diabetes, including diabetic polyneuropathy (DPN), the most common type of polyneuropathy. Oxidative stress is considered the main reason for the cellular pathology development in diabetes mellitus, which determines the use of antioxidants for the DPN treatment. Alpha-lipoic acid (ALA), a natural fat-soluble antioxidant, is the most effective drug for reducing DPN symptoms. Furthermore, the symptom-modifying effect of ALA has been shown in numerous randomized controlled trials. The article discusses the possible disease-modifying effect of ALA.

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5

Galante, Iv. "A. Bakk & Gh. Tamasescu Ueber die Aetiologie und Pathogenese der Epilepsie und deren Therapie. Wiener Med. W. No. 17, 1933." Kazan medical journal 29, no. 5-6 (January 12, 2022): 489. http://dx.doi.org/10.17816/kazmj89620.

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Bakk and Tamasescu (A. Bakk Gh. Tamasescu Ueber die Aetiologie und Pathogenese der Epilepsie und deren Therapie. Wiener Med. W. No. 17, 1933) give a good concise overview of the etiology, pathogenesis and treatment of epilepsy. Epilepsy is an organic syndrome with a different etiology and multiple pathogenetic factors, which explains that the methods of treatment for epilepsy vary enormously.

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6

A, Abdelmoktader. "Mycobacterial Tuberculosis Epidemiology and Pathogenesis." Virology & Immunology Journal 4, no. 4 (November 19, 2020): 1–7. http://dx.doi.org/10.23880/vij-16000259.

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Mycobacterium tuberculosis (MTB) is an acid fast bacterium (AFB); it has tough cell wall and circular chromosome. It is transmitted through the airborne route and cause tuberculosis (TB). The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries and it is the second most common cause of death from infectious disease after HIV. Organisms deposited mainly in the upper lung zones, kidneys and bones. In persons with intact cell-mediated immunity (CMI), collections of activated T cells and macrophages form granulomas that limit multiplication and spread of the organism. The Status of CMI will determine if the patient will get active or latent TB infection.

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7

Kim, Young Kyoon, and Younsuck Koh. "Pathogenesis." Tuberculosis and Respiratory Diseases 50, no. 5 (2001): 525. http://dx.doi.org/10.4046/trd.2001.50.5.525.

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8

Witz, Craig, and Robert Schenken. "Pathogenesis." Seminars in Reproductive Medicine 15, no. 03 (August 1997): 199–208. http://dx.doi.org/10.1055/s-2008-1068749.

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9

Gollnick, Harald P. M., Christos C. Zouboulis, Hirohiko Akamatsu, Ichiro Kurokawa, and Anja Schulte. "Pathogenesis and Pathogenesis Related Treatment of Acne." Journal of Dermatology 18, no. 9 (September 1991): 489–99. http://dx.doi.org/10.1111/j.1346-8138.1991.tb03122.x.

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10

Bilalova, K. A., and L. A. Yusupova. "ROSACEA: FEATURES OF PATHOGENESIS AND THERAPY." European Journal of Natural History, no. 2 2022 (2022): 18–21. http://dx.doi.org/10.17513/ejnh.34252.

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11

Tuor, Paula, and Jenkins Zhao. "Pathogenesis of Brain: Autism Spectrum Disorders." Neuroscience and Neurological Surgery 2, no. 2 (April 20, 2018): 01–02. http://dx.doi.org/10.31579/2578-8868/029.

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Autism spectrum disorders (ASDs) affect as many as 1 in 45 children and are characterized by deficits in sociability and communication, as well as stereotypic movements. Many children also show severe anxiety.

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12

Syabbalo, Nightingale. "Severe Neutrophilic Asthma: Pathogenesis and Treatment." Journal of Thoracic Disease and Cardiothoracic Surgery 3, no. 1 (January 15, 2022): 01–13. http://dx.doi.org/10.31579/2693-2156/030.

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Asthma is a common chronic airway disease affecting about 358 million people worldwide, and an estimated 7 million children globally. Approximately 10% of patients with asthma have severe refractory disease, which is difficult to control on high doses of inhaled corticosteroids and other modifiers. Among these, are patients with severe neutrophilic asthma. Neutrophilic asthma is a severe phenotype of asthma, characterized by frequent exacerbations, persistent airway obstruction, and poor lung function. Immunopathologically, it is characterized by the presence of high levels of neutrophils in the airways and lungs. Interleukin-17 produced by Th17 cells, plays a key role in the pathogenesis of neutrophilic asthma by expressing the secretion of chemoattractant cytokines and chemokines for the recruitment, and activation of neutrophils. Interleukin-8 is a powerful chemoattractant and activator of neutrophils. Activated neutrophils produce an oxidative burst, releasing multiple reactive oxygen species, proteinases, cytokines, which cause airway epithelial cell injury, inflammation, airway hyperresponsiveness, and remodeling. Furthermore, exasperated neutrophils due to viral, bacterial or fungal infections, and chemical irritants can release extracellular nucleic acids (DNA), designated as NETs (neutrophil extracellular traps), which are more toxic to the airway epithelial cells, and orchestrate airway inflammation, and release alarmin cytokines. Dysregulated NETs formation is associated with severe asthma. Most patients with neutrophilic asthma are unresponsive to the standard of care, including high dose inhaled corticosteroids, and to targeted biologics, such as mepolizumab, and dupilumab, which are very effective in treating eosinophilic asthma. There is unmet need to explore for novel biologics for the treatment of neutrophilic asthma, and in refining therapies, such as bronchial thermoplasty.

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13

O.A., Babadjanov, and Pulatova S.X. "ACNE: ETIOLOGY, PATHOGENESIS AND MODERN THERAPY." International Journal of Medical Sciences And Clinical Research 03, no. 03 (March 1, 2023): 46–50. http://dx.doi.org/10.37547/ijmscr/volume03issue03-07.

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14

HAYASHI, Koichi. "Pathogenesis of Hypertension -Kidney as a Pathogenetic Organ of Hypertension." Internal Medicine 40, no. 2 (2001): 153–56. http://dx.doi.org/10.2169/internalmedicine.40.153.

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15

Smith, Laurie D., and Thomas A. Ficht. "Pathogenesis ofBrucella." Critical Reviews in Microbiology 17, no. 3 (January 1990): 209–30. http://dx.doi.org/10.3109/10408419009105726.

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16

Garcia, Sonia Arely, Vincent Y. Ng, Masahiro Iwamoto, and Motomi Enomoto-Iwamoto. "Osteochondroma Pathogenesis." American Journal of Pathology 191, no. 12 (December 2021): 2042–51. http://dx.doi.org/10.1016/j.ajpath.2021.08.003.

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17

Haidar, Ruvin. "Microbial Pathogenesis." International Journal of Health Sciences and Research 11, no. 12 (December 20, 2021): 217–19. http://dx.doi.org/10.52403/ijhsr.20211228.

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For a pathogenic microbe to cause disease in a susceptible host, it must gain access to that host first. The pathogenicity of a microbe is determined by the virulence factors alongside other innate mechanisms. Apart from the initiation of infection, these virulence factors also enable the pathogenic microorganism to survive in the new environment within the susceptible host. They also enable the pathogenic microorganism to invade the host, colonize, and evade the host defense mechanisms. These virulence factors include; invasins, capsules, siderophores, adhesins, enzymes, endotoxins, and exotoxins. Key words: Pathogenicity factors and Pathological effect on cells.

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18

Horwitz, Ralph I., Burton H. Singer, Allison Hayes-Conroy, Mark R. Cullen, McKayla Mawn, Katharine Colella, and Ida Sim. "Biosocial Pathogenesis." Psychotherapy and Psychosomatics 91, no. 2 (2022): 73–77. http://dx.doi.org/10.1159/000521567.

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19

Johnson, Cydney, Virginia Hargest, Valerie Cortez, Victoria Meliopoulos, and Stacey Schultz-Cherry. "Astrovirus Pathogenesis." Viruses 9, no. 1 (January 22, 2017): 22. http://dx.doi.org/10.3390/v9010022.

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20

Eyre, David, and David J. Schurman. "Pathogenesis/Homeostasis." Clinical Orthopaedics and Related Research 427 (October 2004): S104. http://dx.doi.org/10.1097/01.blo.0000144978.73030.b7.

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21

Milner, Danny A. "Malaria Pathogenesis." Cold Spring Harbor Perspectives in Medicine 8, no. 1 (May 22, 2017): a025569. http://dx.doi.org/10.1101/cshperspect.a025569.

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22

Scott, J. R. "Scrapie pathogenesis." British Medical Bulletin 49, no. 4 (October 1993): 778–91. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072646.

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23

Moayeri, Mahtab, Stephen H. Leppla, Catherine Vrentas, Andrei P. Pomerantsev, and Shihui Liu. "Anthrax Pathogenesis." Annual Review of Microbiology 69, no. 1 (October 15, 2015): 185–208. http://dx.doi.org/10.1146/annurev-micro-091014-104523.

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24

Fauci, Anthony S. "Cellular Pathogenesis." AIDS Research and Human Retroviruses 7, no. 2 (February 1991): 202–15. http://dx.doi.org/10.1089/aid.1991.7.202.

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25

Miller, L., M. Good, and G. Milon. "Malaria pathogenesis." Science 264, no. 5167 (June 24, 1994): 1878–83. http://dx.doi.org/10.1126/science.8009217.

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26

FRITSCH, P. "WS102 Pathogenesis." Journal of the European Academy of Dermatology and Venereology 9 (September 1997): S100. http://dx.doi.org/10.1016/s0926-9959(97)89260-4.

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27

Ross, Christopher A. "Polyglutamine Pathogenesis." Neuron 35, no. 5 (August 2002): 819–22. http://dx.doi.org/10.1016/s0896-6273(02)00872-3.

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28

Karumanchi, S. Ananth, and Marshall D. Lindheimer. "Preeclampsia Pathogenesis." Hypertension 51, no. 4 (April 2008): 991–92. http://dx.doi.org/10.1161/hypertensionaha.107.100735.

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29

Paumgartner, G., and T. Sauerbruch. "Gallstones: pathogenesis." Lancet 338, no. 8775 (November 1991): 1117–21. http://dx.doi.org/10.1016/0140-6736(91)91972-w.

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30

Forrester, J. "Uveitis: pathogenesis." Lancet 338, no. 8781 (December 1991): 1498–501. http://dx.doi.org/10.1016/0140-6736(91)92309-p.

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31

Nowak, Martin A. "AIDS Pathogenesis." Journal of Acquired Immune Deficiency Syndromes & Human Retrovirology 10, Supplement (1995): S6. http://dx.doi.org/10.1097/00042560-199510001-00002.

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32

Buller, R. M., and G. J. Palumbo. "Poxvirus pathogenesis." Microbiological Reviews 55, no. 1 (1991): 80–122. http://dx.doi.org/10.1128/mmbr.55.1.80-122.1991.

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33

Buller, R. M., and G. J. Palumbo. "Poxvirus pathogenesis." Microbiological Reviews 55, no. 1 (1991): 80–122. http://dx.doi.org/10.1128/mr.55.1.80-122.1991.

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34

Edlin, Gordon. "AIDS Pathogenesis." Nature Biotechnology 6, no. 2 (February 1988): 217. http://dx.doi.org/10.1038/nbt0288-217b.

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35

Jackson, Alan C. "Rabies pathogenesis." Journal of Neurovirology 8, no. 4 (January 2002): 267–69. http://dx.doi.org/10.1080/13550280290100725.

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36

Nowak, Martin, and Robert M. May. "AIDS pathogenesis." AIDS 7 (January 1992): S3—S18. http://dx.doi.org/10.1097/00002030-199201001-00002.

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37

Nowak, Martin, and Robert M. May. "AIDS pathogenesis." AIDS 7 (January 1993): S3—S18. http://dx.doi.org/10.1097/00002030-199301001-00002.

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38

Ross, Christopher A., Jonathan D. Wood, Gabriele Schilling, Matthew F. Peters, Frederick C. Nucifora, Jillian K. Cooper, Alan H. Sharp, Russell L. Margolis, and David R. Borchelt. "Polyglutamine pathogenesis." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1386 (June 29, 1999): 1005–11. http://dx.doi.org/10.1098/rstb.1999.0452.

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Анотація:

An increasing number of neurodegenerative disorders have been found to be caused by expanding CAG triplet repeats that code for polyglutamine. Huntington's disease (HD) is the most common of these disorders and dentato-rubral-pallidoluysian atrophy (DRPLA) is very similar to HD, but is caused by mutation in a different gene, making them good models to study. In this review, we will concentrate on the roles of protein aggregation, nuclear localization and proteolytic processing in disease pathogenesis. In cell model studies of HD, we have found that truncated N-terminal portions of huntingtin (the HD gene product) with expanded repeats form more aggregates than longer or full length huntingtin polypeptides. These shorter fragments are also more prone to aggregate in the nucleus and cause more cell toxicity. Further experiments with huntingtin constructs harbouring exogenous nuclear import and nuclear export signals have implicated the nucleus in direct cell toxicity. We have made mouse models of HD and DRPLA using an N-terminal truncation of huntingtin (N171) and full-length atrophin-1 (the DRPLA gene product), respectively. In both models, diffuse neuronal nuclear staining and nuclear inclusion bodies are observed in animals expressing the expanded glutamine repeat protein, further implicating the nucleus as a primary site of neuronal dysfunction. Neuritic pathology is also observed in the HD mice. In the DRPLA mouse model, we have found that truncated fragments of atrophin-1 containing the glutamine repeat accumulate in the nucleus, suggesting that proteolysis may be critical for disease progression. Taken together, these data lead towards a model whereby proteolytic processing, nuclear localization and protein aggregation all contribute to pathogenesis.

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39

Cantor, Jerome O., and Gerard M. Turino. "COPD Pathogenesis." Chest 155, no. 2 (February 2019): 266–71. http://dx.doi.org/10.1016/j.chest.2018.07.030.

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40

Dushku, Nicholas. "Pterygia Pathogenesis." Archives of Ophthalmology 119, no. 5 (May 1, 2001): 695. http://dx.doi.org/10.1001/archopht.119.5.695.

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41

Ahn, Christine S., and William W. Huang. "Rosacea Pathogenesis." Dermatologic Clinics 36, no. 2 (April 2018): 81–86. http://dx.doi.org/10.1016/j.det.2017.11.001.

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42

Bespalov, Vladimir G., and Elizaveta I. Kovalevskaya. "Modern conceptions of etiology and pathogenesis of benign breast disease: the possibilities of pathogenetic treatment." Gynecology 21, no. 1 (February 15, 2019): 52–58. http://dx.doi.org/10.26442/20795696.2019.1.190217.

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Relevance. The review article is devoted to modern conceptions of etiology and pathogenesis of benign breast disease (BBD), a common female pathology, as well as the pathogenetic treatment of BBD. Aim. Substantiation of the new possibilities of the pathogenetic treatment of BBD. Materials and methods. It was conducted the analysis of domestic and world literature in the following areas: etiology, pathogenesis, treatment of BBD, prevention of breast cancer (BC). Results. Dozens of etiological factors of various natures cause BBD: genetic, reproductive, hormonal, gynecological diseases, extragenital pathology, environment and lifestyle, medical interventions. The etiological factors of BBD mostly coincide with the risk factors of BC. The lack of progesterone, the predominance of estradiol and chronic hyperestrogenemia, leading to hyperproliferation of the ductal and lobular epithelium of the mammary glands, underlie the pathogenesis of BBD. The pathogenesis of proliferative forms of BBD and BC have common features. In patients with proliferative and precancerous forms of BBD, the risk of BC increases significantly. Chronic iodine deficiency is one of the common pathogenetic pathways for the development of BBD. The drug mamoclam containing organically bound iodine from laminaria thallus is an effective and safe remedy for the pathogenetic treatment of BBD. Conclusion. Pathogenetic treatment of BBD not only improves the quality of life of patients, but also reduces the risk of BC.

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43

K.Z., Kadirov, and Isroilov R.I. "ETHIO-PATHOGENESIS OF POUND DESTROYMENT IN CHILDREN." American Journal of Medical Sciences and Pharmaceutical Research 6, no. 2 (February 1, 2024): 75–82. http://dx.doi.org/10.37547/tajmspr/volume06issue02-10.

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Infectious diseases are one of the most serious problems because they are the most widespread and the leading cause of death. Although significant advances have been made over the past decades in addressing this problem, this statement is still true today. Sepsis is the leading cause of death in critical care patients. It develops in 750000 people each year and more than 210000 of them die. Progress in the study of the pathophysiology and genetic basis of the individual response to sepsis has changed the common understanding of this syndrome, and some therapeutic interventions used in recent years have demonstrated efficacy; however, the problem of intensive care is still quite acute and requires further research.

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44

Rohilla, Lakshita, Karandeep Singh, and Abhijit Garg. "Intranasal Malignantmelanoma: Pathogenesis Epidemiology and Clinical Insight." International Journal of Science and Research (IJSR) 12, no. 9 (September 5, 2023): 740–44. http://dx.doi.org/10.21275/sr23907100157.

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45

Borozdenko, Denis A., Vladislava I. Bogorodova, Nina M. Kiseleva, and Vadim V. Negrebetsky. "Parkinson’s disease: epidemiology and pathogenesis." Medical Journal of the Russian Federation 27, no. 2 (July 23, 2021): 183–94. http://dx.doi.org/10.17816/0869-2106-2021-27-2-183-194.

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Анотація:

This review presents data on the etiology, epidemiology, and pathogenesis of Parkinsons disease from National Center for Biotechnology Information (NCBI), eLibrary, CyberLeninka, and from monographs and textbooks. The prevalence, classification, genetic variability, main pathogenetic links, and potential disease development mechanisms are described. Both classic Parkinsons disease and variable manifestations of parkinsonism are considered. The factors that contribute to disease progression and inhibit its development are described. The main hypotheses of the pathogenetic mechanisms of Parkinsons disease are presented. These are protein misfolding, mitochondrial dysfunction, impaired protein purification systems, neuroinflammation, and pathology of the gut-brain axis.

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46

Varghese, Smitha Ancy. "Secondary lymphedema: Pathogenesis." Journal of Skin and Sexually Transmitted Diseases 3 (April 6, 2021): 7–15. http://dx.doi.org/10.25259/jsstd_3_2020.

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Secondary lymphedema follows an acquired defect in the lymphatic system. The common causes leading to a defective lymphatic function include infection, inflammation, malignancy, trauma, obesity, immobility, and therapeutic interventions. Understanding the pathogenesis of lymphedema is of prime importance in offering effective treatment. The pathogenetic mechanisms such as lymphatic valvular insufficiency, obliteration/ disruption of lymphatic vessels, and decreased lymphatic contractility aggravate lymphatic hypertension and lymphstasis. Accumulation of lymph, interstitial fluid, proteins, and glycosaminoglycans within the skin and subcutaneous tissue eventually stimulates collagen production by fibroblasts, causes disruption of elastic fibers, and activates keratinocytes, fibroblasts, and adipocytes. These result in thickening of skin and cause fibrosis of subcutaneous tissue. However, the sequence of these pathomechanisms, their inter-relationship and progression vary depending on the specific etiology of the lymphedema. In this article, we discuss the possible cellular and molecular mechanisms involved in the pathogenesis. Further studies to delineate the exact sequence of pathogenic processes surrounding the primary triggering event can help to formulate tailored therapeutic approaches.

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47

Varghese, Smitha Ancy. "Secondary lymphedema: Pathogenesis." Journal of Skin and Sexually Transmitted Diseases 3 (April 6, 2021): 7–15. http://dx.doi.org/10.25259/jsstd_3_2021.

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Secondary lymphedema follows an acquired defect in the lymphatic system. The common causes leading to a defective lymphatic function include infection, inflammation, malignancy, trauma, obesity, immobility, and therapeutic interventions. Understanding the pathogenesis of lymphedema is of prime importance in offering effective treatment. The pathogenetic mechanisms such as lymphatic valvular insufficiency, obliteration/ disruption of lymphatic vessels, and decreased lymphatic contractility aggravate lymphatic hypertension and lymphstasis. Accumulation of lymph, interstitial fluid, proteins, and glycosaminoglycans within the skin and subcutaneous tissue eventually stimulates collagen production by fibroblasts, causes disruption of elastic fibers, and activates keratinocytes, fibroblasts, and adipocytes. These result in thickening of skin and cause fibrosis of subcutaneous tissue. However, the sequence of these pathomechanisms, their inter-relationship and progression vary depending on the specific etiology of the lymphedema. In this article, we discuss the possible cellular and molecular mechanisms involved in the pathogenesis. Further studies to delineate the exact sequence of pathogenic processes surrounding the primary triggering event can help to formulate tailored therapeutic approaches.

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